Cited by 183interferon and immune responsesAcute Myeloid Leukemia ResearchImmunodeficiency and Autoimmune Disorders
The DOI matches its Crossref record; 72 of the 72 references it cites were found in a registry or an index; none of the 124 sources its claims cite is checked for support yet.
Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells
Abstract
Interferon (IFN) consensus sequence binding protein (ICSBP)/IFN regulatory factor (IRF)-8 is an IFNgamma-inducible transcription factor of the IRF family and regulates transcription through multiple target DNA elements, such as IFN-stimulated response element (ISRE), Ets/IRF composite element, and IFN-gamma activation site (GAS). ICSBP(-/-) mice are immunodeficient and susceptible to various pathogens. They have defects in the macrophage function, including the ability to induce interleukin-12 (IL-12) p40 and some IFN-gamma-responsible genes. In addition, ICSBP(-/-) mice develop a chronic myelogenous leukemia (CML)-like syndrome, where a systemic expansion of granulocytes is followed by a fatal blast crisis. ICSBP(-/-) mice harbor an increased number of myeloid progenitor cells, and the -/- progenitors preferentially give rise to granulocytes, although they cannot efficiently generate another descendant of the myeloid lineage, macrophages. Studies with myeloid progenitor cells have shown that ICSBP drives their differentiation toward macrophage, whereas it inhibits granulocyte differentiation. Furthermore, myeloid cells from ICSBP(-/-) mice are resistant to apoptosis. These results illustrate the mechanism by which the loss of ICSBP leads to immunodeficiency and CML-like syndrome and suggest ICSBP's critical role in the development of myeloid cells.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
ICSBP/IRF-8 is an IFN-γ–inducible transcription factor of the IRF family that regulates myeloid cell development, acting as either a repressor or activator depending on the target DNA element. Loss of ICSBP in mice causes immunodeficiency (defective macrophage/IL-12 function) and a chronic myelogenous leukemia (CML)-like syndrome.
Key findings
- ICSBP⁻/⁻ mice are immunodeficient and susceptible to pathogens controlled by type II IFN (vaccinia, lymphocytic choriomeningitis virus, *Listeria monocytogenes*, *Yersinia enterocolitica*, *Leishmania major*, *Toxoplasma gondii*), but survive vesicular stomatitis virus or influenza A.
- ICSBP⁻/⁻ mice develop a CML-like syndrome: systemic expansion/infiltration of granulocytes (predominantly mature neutrophils) in essentially 100% of mice, with lymphadenopathy and hepatosplenomegaly; approximately 33% of ICSBP⁻/⁻ and 9% of ICSBP⁺/⁻ mice died by 50 weeks of age with features of blast crisis, including leukocytosis (>100,000/μl).
- ICSBP directs myeloid progenitors toward macrophage differentiation and inhibits granulocyte growth/differentiation; ICSBP⁻/⁻ myeloid cells show reduced spontaneous apoptosis and reduced sensitivity to DNA-damage–induced apoptosis.
- ICSBP activates IL-12 p40 transcription (via the Ets site, with IRF-1 synergy) and potentiates Stat1-dependent activation of IFN-γ–responsive GAS-containing promoters; ICSBP⁻/⁻ macrophages are defective in inducing FcγRI and iNOS.
Methods
- Narrative review synthesizing published and unpublished work on ICSBP/IRF-8, its structure, target elements, interacting proteins, and role in myeloid development.
- Evidence drawn from ICSBP⁻/⁻ and ICSBP⁺/⁻ mice, established ICSBP⁻/⁻ myeloid progenitor cell lines (e.g., Tot2), retroviral ICSBP transduction, colony-forming assays with GM-CSF/G-CSF/M-CSF, DNA affinity binding assays, and transfected luciferase reporters.
- No new primary data or formal meta-analysis are presented; the paper is a synthesis of cited studies.
Limitations
- Stated: many studies relied on activities of transfected reporters containing ISRE or EICE, so it remains important to determine whether ICSBP regulates endogenous genes through these elements; immediate target genes that trigger differentiation in progenitor cells have not been identified.
- Stated: some cited observations are unpublished (e.g., ICSBP expression in Lin⁻ progenitors, additional IL-12 p40 promoter element, TEL interaction, dendritic cell maturation).
- Evident from the text: as a review, conclusions depend on the cited primary studies, and several mechanistic claims (e.g., ICSBP–IRF-4 compensation) are proposed as possibilities rather than demonstrated.
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Integrity signals
Registry
Crossref · 10.1089/107999002753452755
Cites
72 of 72 references verified0 citation errors · 0 not checkable
Statistics
Nothing to recompute.
Verification
Claims the paper makes
62 Not checked yet · 20 Own interpretation · 4 Own result · 2 No basis given
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Recently, we found that ICSBP is expressed in lineage marker-negative (Lin 2 ) hematopoietic progenitor cells in bone marrow.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In contrast, apoptosis in ICSBP 2 / 2 thymocytes was unaffected.”
What the sources say
- Not checked yetcites [56] 56. GABRIELE, L., PHUNG, J., FUKUMOTO, J., SEGAL, D., WANG, I.M., GIANNAKAKOU, P., GIESE, N.A., OZATO, K., and MORSE, H.C., 3rd (1999). Regulation of apoptosis in myeloid cells by interferon consensus sequence-binding protein. J. Exp. Med. 190, 411-421. source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Cells overexpressing ICSBP had enhanced expression of caspase-3 precursor protein and decreased expression of Bcl-X(L).”
What the sources say
- Not checked yetcites [56] 56. GABRIELE, L., PHUNG, J., FUKUMOTO, J., SEGAL, D., WANG, I.M., GIANNAKAKOU, P., GIESE, N.A., OZATO, K., and MORSE, H.C., 3rd (1999). Regulation of apoptosis in myeloid cells by interferon consensus sequence-binding protein. J. Exp. Med. 190, 411-421. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Overexpression of ICSBP in the human U937 myelomonoblastic leukemia cell line enhanced the rate of spontaneous apoptosis and increased the sensitivity to apoptosis induced by etoposide, LPS plus ATP, or rapamycin.”
What the sources say
- Not checked yetcites [56] 56. GABRIELE, L., PHUNG, J., FUKUMOTO, J., SEGAL, D., WANG, I.M., GIANNAKAKOU, P., GIESE, N.A., OZATO, K., and MORSE, H.C., 3rd (1999). Regulation of apoptosis in myeloid cells by interferon consensus sequence-binding protein. J. Exp. Med. 190, 411-421. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Cells overexpressing ICSBP had enhanced expression of caspase-3 precursor protein and decreased expression of Bcl-X(L).”
What the sources say
- Not checked yetcites [56] 56. GABRIELE, L., PHUNG, J., FUKUMOTO, J., SEGAL, D., WANG, I.M., GIANNAKAKOU, P., GIESE, N.A., OZATO, K., and MORSE, H.C., 3rd (1999). Regulation of apoptosis in myeloid cells by interferon consensus sequence-binding protein. J. Exp. Med. 190, 411-421. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Overexpression of ICSBP in the human U937 myelomonoblastic leukemia cell line enhanced the rate of spontaneous apoptosis and increased the sensitivity to apoptosis induced by etoposide, LPS plus ATP, or rapamycin.”
What the sources say
- Not checked yetcites [56] 56. GABRIELE, L., PHUNG, J., FUKUMOTO, J., SEGAL, D., WANG, I.M., GIANNAKAKOU, P., GIESE, N.A., OZATO, K., and MORSE, H.C., 3rd (1999). Regulation of apoptosis in myeloid cells by interferon consensus sequence-binding protein. J. Exp. Med. 190, 411-421. source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“Myeloid cells (Gr1 1 as well as Mac1 1 cells) from ICSBP 2 / 2 were shown to exhibit reduced spontaneous apoptosis.”
What the sources say
- Not checked yetcites [56] 56. GABRIELE, L., PHUNG, J., FUKUMOTO, J., SEGAL, D., WANG, I.M., GIANNAKAKOU, P., GIESE, N.A., OZATO, K., and MORSE, H.C., 3rd (1999). Regulation of apoptosis in myeloid cells by interferon consensus sequence-binding protein. J. Exp. Med. 190, 411-421. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Further, in ICSBP 2 / 2 cells, there was a significant decrease in the sensitivity to apoptosis induced by DNA damage. (56)”
What the sources say
- Not checked yetcites [56] 56. GABRIELE, L., PHUNG, J., FUKUMOTO, J., SEGAL, D., WANG, I.M., GIANNAKAKOU, P., GIESE, N.A., OZATO, K., and MORSE, H.C., 3rd (1999). Regulation of apoptosis in myeloid cells by interferon consensus sequence-binding protein. J. Exp. Med. 190, 411-421. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“although studies of Egr-1 2 / 2 mice indicated the presence of redundant mechanisms capable of compensating Egr-1 activity. (58)”
What the sources say
- Not checked yetcites [58] 58. LEE, S.L., WANG, Y., and MILBRANDT, J. (1996). Unimpaired macrophage differentiation and activation in mice lacking the zinc finger transplantation factor NGFI-A (EGR1). Mol. Cell. Biol. 16, 4566-4572. source
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“Programmed cell death induced by etoposide was specifically blocked by peptides inhibitory for the caspase-1 or caspase-3 subfamilies of caspases.”
What the sources say
- Not checked yetcites [56] 56. GABRIELE, L., PHUNG, J., FUKUMOTO, J., SEGAL, D., WANG, I.M., GIANNAKAKOU, P., GIESE, N.A., OZATO, K., and MORSE, H.C., 3rd (1999). Regulation of apoptosis in myeloid cells by interferon consensus sequence-binding protein. J. Exp. Med. 190, 411-421. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“It is interesting to note that ICSBP induces a zinc finger transcription factor Egr-1 that has been implicated in macrophage differentiation, (57)”
What the sources say
- Not checked yetcites [57] 57. NGUYEN, H.Q., HOFFMAN, L.B., and LIEBERMANN, D.A. - (1993). The zinc finger transcription factor Egr-1 is essential for and restricts differentiation along the macrophage lineage. Cell 72, 197-209. source
plaindirect- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Our recent data also show that ICSBP plays a critical role in the maturation of dendritic cells (H. Tsujimura, T.T., and K.O., submitted).”
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“ICSBP was also shown to interact with E47 (encoded by the E2A gene) on the element composed of IRS-like sequence and the E2A binding site found in the Ig k 3 9 enhancer to activate transcription, again like IRF-4. (5,32)”
What the sources say
- Not checked yetcites [5] 5. MERARO, D., HASHMUELI, S., KOREN, B., AZRIEL, A., OUMARD, A., KIRCHHOFF, S., HAUSER, H., NAGULAPALLI, S., ATCHISON, M.L., and LEVI, B.-Z. (1999). Proteinprotein and DNA-protein interactions affect the activity of lymphoid-specific IFN regulatory factors. J. Immunol. 163, 64686478. source
- Not checked yetcites [32] 32. NAGULAPALLI, S., and ATCHISON, M.L. (1998). Transcription factor Pip can enhance DNA binding by E47, leading to transcriptional synergy involving multiple protein domains. Mol. Cell. Biol. 18, 4639-4650. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Recent studies indicate that ICSBP can act on a wide range of target elements even beyond the IRS, such as the Ets site in IL-12 p40 promoter and the IFNg activation site (GAS). (15,34)”
What the sources say
- Not checked yetcites [15] 15. WANG, I.M., CONTURSI, C., MASUMI, A., MA, X., TRINCHIERI, G., and OZATO, K. (2000). An IFN-gamma-inducible transcription factor, IFN consensus sequence binding protein (ICSBP), stimulates IL-12 p40 expression in macrophages. J. Immunol. 165, 271-279. source
- Not checked yetcites [34] 34. CONTURSI, C., WANG, I.M., GABRIELE, L., GADINA, M., O'SHEA, J., MORSE, H.C., 3rd, and OZATO, K. (2000). IFN consensus sequence binding protein potentiates Stat1-dependent activation of IFNgamma-responsive promoters in macrophages. Proc. Natl. Acad. Sci. USA 97, 91-96. source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Subsequent studies have shown that ICSBP is a transcriptional repressor acting through the IFN-stimulated response element (ISRE). (6,20,21)”
What the sources say
- Not checked yetcites [6] 6. WEISZ, A., MARX, P., SHARF, R., APPELLA, E., DRIGGERS, P.H., OZATO, K., and LEVI, B.-Z. (1992). Human interferon consensus sequence binding protein is a negative regulator of enhancer elements common to interferon-inducible genes. J. Biol. Chem. 267, 25589-25596. source
- Not checked yetcites [20] 20. NELSON, N., MARKS, M.S., DRIGGERS, P.H., and OZATO, K. (1993). Interferon consensus sequence-binding protein, a member of the interferon regulatory factor family, suppresses interferon-induced gene transcription. Mol. Cell. Biol. 13, 588-599. source
- Not checked yetcites [21] 21. WEISZ, A., KIRCHHOFF, S., and LEVI, B.-Z. (1994). IFN consensus sequence binding protein (ICSBP) is a conditional repressor of IFN inducible promoters. Int. Immunol. 6, 1125-1131. source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Clearly, ICSBP can act either as a repressor or as an activator, depending on the target DNA sequence, presumably by interacting with different proteins.”
boostedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“It has been reported that ICSBP is constitutively phosphorylated on tyrosine (Tyr) residues in vivo .”
What the sources say
- Not checked yetcites [35] 35. SHARF, R., MERARO, D., AZRIEL, A., THORNTON, A.M., OZATO, K., PETRICOIN, E.F., LARNER, A.C., SCHAPER, F., HAUSER, H., and LEVI, B.-Z. (1997). Phosphorylation events modulate the ability of interferon consensus sequence binding protein to interact with interferon regulatory factors and to bind DNA. J. Biol. Chem. 272, 9785-9792. source
hedged- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“They have defects in the macrophage function, including the ability to induce interleukin-12 (IL-12) p40 and some IFNg -responsible genes.”
- Also stated in: § ICSBPretrovirus · plain
“Macrophages from ICSBP 2 / 2 mice were found to be defective in inducing some IFNg -responsive genes, such as Fc g receptor I (Fc g RI) and nitric oxide synthase (iNOS) genes.”
What the sources say
- Not checked yetcites [34] 34. CONTURSI, C., WANG, I.M., GABRIELE, L., GADINA, M., O'SHEA, J., MORSE, H.C., 3rd, and OZATO, K. (2000). IFN consensus sequence binding protein potentiates Stat1-dependent activation of IFNgamma-responsive promoters in macrophages. Proc. Natl. Acad. Sci. USA 97, 91-96. source
- Not checked yetcites [40] 40. GIESE, N.A., GABRIELE, L., DOHERTY, T.M., KLINMAN, D.M., TADESSE-HEATH, L., CONTURSI, C., EPSTEIN, S.L., and MORSE, H.C., 3rd (1997). Interferon (IFN) consensus sequence-binding protein, a transcription factor of the IFN regulatory factor family, regulates immune responses in vivo through control of interleukin 12 expression. J. Exp. Med. 186, 1535-1546. source
- Not checked yetcites [41] 41. SCHARTON-KERSTEN, T., CONTURSI, C., MASUMI, A., SHER, A., and OZATO, K. (1997). Interferon consensus sequence binding protein-deficient mice display impaired resistance to intracellular infection due to a primary defect in interleukin 12 p40 induction. J. Exp. Med. 186, 1523-1534. source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Also stated in: § ICSBPretrovirus · plain
In the paper
“The phenotype of ICSBP 2 / 2 mice suggested a previously unpredicted role of ICSBP in myeloid cell development. (37)”
What the sources say
- Not checked yetcites [37] 37. HOLTSCHKE, T., LOHLER, J., KANNO, Y., FEHR, T., GIESE, N., ROSENBAUER, F., LOU, J., KNOBELOCH, K.P., GABRIELE, L., WARING, J.F., BACHMANN, M.F., ZINKERNAGEL, R.M., MORSE, H.C., 3rd, OZATO, K., and HORAK, I. (1996). Immunodeficiency and chronic myelogenous leukemia-like syndrome in mice with a targeted mutation of the ICSBP gene. Cell 87, 307-317. source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“It was also shown that ICSBP 2 / 2 hematopoietic progenitor cells display significantly reduced adhesion to fibronectin. (49)”
What the sources say
- Not checked yetcites [49] 49. SCHELLER, M., FOERSTER, J., HEYWORTH, C.M., WARING, J.F., LOHLER, J., GILMORE, G.L., SHADDUCK, R.K., DEXTER, T.M., and HORAK, I. (1999). Altered development and cytokine responses of myeloid progenitors in the absence of transcription factor, interferon consensus sequence binding protein. Blood 94, 3764-3771. source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, ICSBP, induced by IFNg /LPS, acts as a principal activator of IL-12 p40 transcription in macrophages.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“On the other hand, splenocytes or purified CD4 1 T cells from ICSBP 2 / 2 mice could produce IFNg in vitro in response to concanavalin A (ConA), IL-12, or anti-CD3 plus anti-CD28 antibodies. (40,41,44)”
What the sources say
- Not checked yetcites [40] 40. GIESE, N.A., GABRIELE, L., DOHERTY, T.M., KLINMAN, D.M., TADESSE-HEATH, L., CONTURSI, C., EPSTEIN, S.L., and MORSE, H.C., 3rd (1997). Interferon (IFN) consensus sequence-binding protein, a transcription factor of the IFN regulatory factor family, regulates immune responses in vivo through control of interleukin 12 expression. J. Exp. Med. 186, 1535-1546. source
- Not checked yetcites [41] 41. SCHARTON-KERSTEN, T., CONTURSI, C., MASUMI, A., SHER, A., and OZATO, K. (1997). Interferon consensus sequence binding protein-deficient mice display impaired resistance to intracellular infection due to a primary defect in interleukin 12 p40 induction. J. Exp. Med. 186, 1523-1534. source
- Not checked yetcites [44] 44. WU, C.Y., MAEDA, H., CONTURSI, C., OZATO, K., and SEDER, R.A. (1999). Differential requirement of IFN consensus sequence binding protein for the production of IL-12 and induction of Th1-type cells in response to IFN-gamma. J. Immunol. 162, 807-812. source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“It has been reported that ICSBP expression is reduced in CML and acute myeloid leukemia (AML) patients. (50)”
What the sources say
- Not checked yetcites [50] 50. SCHMIDT, M., NAGEL, S., PROBA, J., THIEDE, C., RITTER, M., WARING, J.F., ROSENBAUER, F., HUHN, D., WITTIG, B., HORAK, I., and NEUBAUER, A. (1998). Lack of interferon consensus sequence binding protein (ICSBP) transcripts in human myeloid leukemias. Blood 91, 22-29. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Together, ICSBP regulates multiple stages of immune responses in macrophages.”
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The reduced apoptosis may contribute to quantitative and qualitative changes in the ICSBP 2 / 2 myeloid progenitor cells, as well as to their progeny, further promoting the overgeneration of granulocytes (Fig. 4).”
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Another piece of evidence pointing to a defect in responding to IFNg in ICSBP 2 / 2 macrophages is that they produce a reduced amount of reactive oxygen intermediates on IFNg stimulation. (38)”
What the sources say
- Not checked yetcites [38] 38. FEHR, T., SCHOEDON, G., ODERMATT, B., HOLTSCHKE, T., SCHNEEMANN, M., BACHMANN, M.F., MAK, T.W., HORAK, I., and ZINKERNAGEL, R.M. (1997). Crucial role of interferon consensus sequence binding protein, but neither of interferon regulatory factor 1 nor of nitric oxide synthesis for protection against murine listeriosis. J. Exp. Med. 185, 921-931. source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These results indicate that ICSBP modulates survival of myeloid cells by regulating the expression of apoptosis-related genes.”
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Consistent with this, EICE-like elements in the promoters of the CYBB and NCF2 genes were shown to be bound and activated by ICSBP together with PU.1 and IRF-1 in U937 cells. (28,48)”
What the sources say
- Not checked yetcites [28] 28. EKLUND, E.A, JALAVA, A., and KAKAR, R. (1998). PU.1, interferon regulatory factor 1, and interferon consensus sequencebinding protein cooperate to increase gp91 (phox) expression. J. Biol. Chem. 273, 13957-13965. source
- Not checked yetcites [48] 48. EKLUND, E.A., and KAKAR, R. (1999). Recruitment of CREBbinding protein by PU.1, IFN-regulatory factor-1, and the IFN consensus sequence-binding protein is necessary for IFN-gammainduced p67 phox and gp91 phox expression. J. Immunol. 163, 60956105. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“IL-12 governs production of IFNg in natural killer (NK) cells and CD4 1 T cells.”
What the sources say
- Not checked yetcites [43] 43. STARK, G.R., KERR, I.M., WILLIAMS, B.R., SILVERMAN, R.H., and SCHREIBER, R.D. (1998). How cells respond to interferons. Annu. Rev. Biochem. 67, 227-264. source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“suggesting that the in vivo response to IFNg may be impaired in ICSBP 2 / 2 mice.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In view of the fact that ICSBP and PU.1 cooperate to activate a number of myeloid-specific gene promoters through the EICE, PU.1 is an obvious candidate partner with which ICSBP regulates myeloid cell development.”
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In view of the fact that ICSBP and PU.1 cooperate to activate a number of myeloid-specific gene promoters through the EICE, PU.1 is an obvious candidate partner with which ICSBP regulates myeloid cell development.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“One of the proteins that directly interact with ICSBP is the Ets transcription factor PU.1, which regulates the expression of numerous myeloid-specific genes. (59)”
What the sources say
- Not checked yetcites [59] 59. TENEN, D.G., HROMAS, R., LIGHT, J.D., and ZHANG, D.E. (1997). Transcription factors, normal myeloid development, and leukemia. Blood 90, 489-519. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Further, ICSBP regulates lineage selection of myeloid progenitor cells.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“IRF-4 is similar to ICSBP in structure, interacts with some common partners (PU.1 and E47), and regulates an overlapping set of target promoters. (31,32,63,64)”
What the sources say
- Not checked yetcites [31] 31. EISENBEIS, C.F., SINGH, H., and STORB, U. (1995). Pip, a novel IRF family member, is a lymphoid-specific, PU.1-dependent transcriptional activator. Genes Dev. 9, 1377-1387. source
- Not checked yetcites [32] 32. NAGULAPALLI, S., and ATCHISON, M.L. (1998). Transcription factor Pip can enhance DNA binding by E47, leading to transcriptional synergy involving multiple protein domains. Mol. Cell. Biol. 18, 4639-4650. source
- Not checked yetcites [63] 63. YAMAGATA, T., NISHIDA, J., TANAKA, S., SAKAI, R., MITANI, K., YOSHIDA, M., TANIGUCHI, T., YAZAKI, Y., and HIRAI, H. (1996). A novel interferon regulatory factor family transcription factor, ICSAT/Pip/LSIRF, that negatively regulates the activity of interferon-regulated genes. Mol. Cell. Biol. 16, 12831294. source
- Not checked yetcites [64] 64. BRASS, A.L., KEHRLI, E., EISENBEIS, C.F., STORB, U., and SINGH, H. (1996). Pip, a lymphoid-restricted IRF, contains a regulatory domain that is important for autoinhibition and ternary complex formation with the Etx factor PU.1. Genes Dev. 10, 23352347. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“However, ICSBP and IRF-1 cooperate to activate transcription through some target elements. (15,28,30,48)”
What the sources say
- Not checked yetcites [15] 15. WANG, I.M., CONTURSI, C., MASUMI, A., MA, X., TRINCHIERI, G., and OZATO, K. (2000). An IFN-gamma-inducible transcription factor, IFN consensus sequence binding protein (ICSBP), stimulates IL-12 p40 expression in macrophages. J. Immunol. 165, 271-279. source
- Not checked yetcites [28] 28. EKLUND, E.A, JALAVA, A., and KAKAR, R. (1998). PU.1, interferon regulatory factor 1, and interferon consensus sequencebinding protein cooperate to increase gp91 (phox) expression. J. Biol. Chem. 273, 13957-13965. source
- Not checked yetcites [30] 30. MARECKI, S., RIENDEAU, C.J., LIANG, M.D., and FENTON, M.J. (2001). PU.1 and multiple IFN regulatory factor proteins synergize to mediate transcriptional activation of the human IL-1beta gene. J. Immunol. 166, 6829-6838. source
- Not checked yetcites [48] 48. EKLUND, E.A., and KAKAR, R. (1999). Recruitment of CREBbinding protein by PU.1, IFN-regulatory factor-1, and the IFN consensus sequence-binding protein is necessary for IFN-gammainduced p67 phox and gp91 phox expression. J. Immunol. 163, 60956105. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“IRF-4 is similar to ICSBP in structure, interacts with some common partners (PU.1 and E47), and regulates an overlapping set of target promoters. (31,32,63,64)”
What the sources say
- Not checked yetcites [31] 31. EISENBEIS, C.F., SINGH, H., and STORB, U. (1995). Pip, a novel IRF family member, is a lymphoid-specific, PU.1-dependent transcriptional activator. Genes Dev. 9, 1377-1387. source
- Not checked yetcites [32] 32. NAGULAPALLI, S., and ATCHISON, M.L. (1998). Transcription factor Pip can enhance DNA binding by E47, leading to transcriptional synergy involving multiple protein domains. Mol. Cell. Biol. 18, 4639-4650. source
- Not checked yetcites [63] 63. YAMAGATA, T., NISHIDA, J., TANAKA, S., SAKAI, R., MITANI, K., YOSHIDA, M., TANIGUCHI, T., YAZAKI, Y., and HIRAI, H. (1996). A novel interferon regulatory factor family transcription factor, ICSAT/Pip/LSIRF, that negatively regulates the activity of interferon-regulated genes. Mol. Cell. Biol. 16, 12831294. source
- Not checked yetcites [64] 64. BRASS, A.L., KEHRLI, E., EISENBEIS, C.F., STORB, U., and SINGH, H. (1996). Pip, a lymphoid-restricted IRF, contains a regulatory domain that is important for autoinhibition and ternary complex formation with the Etx factor PU.1. Genes Dev. 10, 23352347. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“IRF-4 is similar to ICSBP in structure, interacts with some common partners (PU.1 and E47), and regulates an overlapping set of target promoters. (31,32,63,64)”
What the sources say
- Not checked yetcites [31] 31. EISENBEIS, C.F., SINGH, H., and STORB, U. (1995). Pip, a novel IRF family member, is a lymphoid-specific, PU.1-dependent transcriptional activator. Genes Dev. 9, 1377-1387. source
- Not checked yetcites [32] 32. NAGULAPALLI, S., and ATCHISON, M.L. (1998). Transcription factor Pip can enhance DNA binding by E47, leading to transcriptional synergy involving multiple protein domains. Mol. Cell. Biol. 18, 4639-4650. source
- Not checked yetcites [63] 63. YAMAGATA, T., NISHIDA, J., TANAKA, S., SAKAI, R., MITANI, K., YOSHIDA, M., TANIGUCHI, T., YAZAKI, Y., and HIRAI, H. (1996). A novel interferon regulatory factor family transcription factor, ICSAT/Pip/LSIRF, that negatively regulates the activity of interferon-regulated genes. Mol. Cell. Biol. 16, 12831294. source
- Not checked yetcites [64] 64. BRASS, A.L., KEHRLI, E., EISENBEIS, C.F., STORB, U., and SINGH, H. (1996). Pip, a lymphoid-restricted IRF, contains a regulatory domain that is important for autoinhibition and ternary complex formation with the Etx factor PU.1. Genes Dev. 10, 23352347. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“One of the proteins that directly interact with ICSBP is the Ets transcription factor PU.1, which regulates the expression of numerous myeloid-specific genes. (59)”
What the sources say
- Not checked yetcites [59] 59. TENEN, D.G., HROMAS, R., LIGHT, J.D., and ZHANG, D.E. (1997). Transcription factors, normal myeloid development, and leukemia. Blood 90, 489-519. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“in light of well-known anti-oncogenic and proapoptotic functions of IRF1 and the oncogenic potential of IRF-2, (61) ICSBP may regulate growth/apoptosis-related genes in myeloid cells by interacting with IRF-1 or IRF-2 or both.”
What the sources say
- Not checked yetcites [61] 61. TANAKA, N., and TANIGUCHI, T. (2000). The interferon regulatory factors and oncogenesis. Semin. Cancer Biol. 10, 73-81. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“ICSBP starts to affect the proliferative potential of myeloid cells at the progenitor cell level.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“ICSBP positively regulates apoptosis in myeloid cells.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
- It may state two separate claims as one. 38
- Probably not a substantial claim. 11
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The expression is relatively high in macrophages and very low in granulocytes (H. Tsujimura, T. Nagamura-Inoue, T.T., and K.O., unpublished observations).”
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“PU.1 2 / 2 mice do not produce mature macrophages and have very few granulocytes. (60)”
What the sources say
- Not checked yetcites [60] 60. SIMON, M.C. (1998). PU.1 and hematopoiesis: lessons learned from gene targeting experiments. Semin. Immunol. 10, 111-118. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Although neither IRF-1 2 / 2 , IRF-2 2 / 2 , nor IRF-1 2 / 2 /IRF-2 2 / 2 mice were reported to have defects in myeloid differentiation,”
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“IRF-4 2 / 2 mice develop progressive generalized lymphadenopathy and have severe defects in B and T lymphocyte function. (65)”
What the sources say
- Not checked yetcites [65] 65. MITTRUCKER, H.W., MATSUYAMA, T., GROSSMAN, A., KUNDIG, T.M., POTTER, J., SHAHINIAN, A., WAKEHAM, A., PATTERSON, B., OHASHI, P.S., and MAK, T.W. (1997). Requirement for the transcription factor LSIRF/IRF4 for mature B and T lymphocyte function. Science 275, 540-543. Address reprint requests to: Dr. Tomohiko Tamura Laboratory of Molecular Growth Regulation National Institute of Child Health and Human Development National Institutes of Health Building 6, Room 416 9000 Rockville Pike Bethesda, MD 20892-2753 Tel: (301) 496-2518 Fax: (301) 480-9354 E-mail: tamurat@mail.nih.gov Accepted 1 August source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“IRF-4 2 / 2 mice develop progressive generalized lymphadenopathy and have severe defects in B and T lymphocyte function. (65)”
What the sources say
- Not checked yetcites [65] 65. MITTRUCKER, H.W., MATSUYAMA, T., GROSSMAN, A., KUNDIG, T.M., POTTER, J., SHAHINIAN, A., WAKEHAM, A., PATTERSON, B., OHASHI, P.S., and MAK, T.W. (1997). Requirement for the transcription factor LSIRF/IRF4 for mature B and T lymphocyte function. Science 275, 540-543. Address reprint requests to: Dr. Tomohiko Tamura Laboratory of Molecular Growth Regulation National Institute of Child Health and Human Development National Institutes of Health Building 6, Room 416 9000 Rockville Pike Bethesda, MD 20892-2753 Tel: (301) 496-2518 Fax: (301) 480-9354 E-mail: tamurat@mail.nih.gov Accepted 1 August source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Recently, we found that another Ets transcription factor, TEL, interacts with ICSBP to be recruited onto the ISRE (C. Gongora, T. Kuwata, T.T., and K.O., submitted for publication).”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“ICSBP 2 / 2 mice are immunodeficient and susceptible to various pathogens.”
- Also stated in: § IMMUNODEFICIENCY OF ICSBP 2 / 2 MICE · plain
“ICSBP 2 / 2 mice were found to display increased susceptibility to infection with various pathogens, control of which requires type II IFN (IFNg )-mediated immunity.”
What the sources say
- Not checked yetcites [37] 37. HOLTSCHKE, T., LOHLER, J., KANNO, Y., FEHR, T., GIESE, N., ROSENBAUER, F., LOU, J., KNOBELOCH, K.P., GABRIELE, L., WARING, J.F., BACHMANN, M.F., ZINKERNAGEL, R.M., MORSE, H.C., 3rd, OZATO, K., and HORAK, I. (1996). Immunodeficiency and chronic myelogenous leukemia-like syndrome in mice with a targeted mutation of the ICSBP gene. Cell 87, 307-317. source
- Not checked yetcites [38] 38. FEHR, T., SCHOEDON, G., ODERMATT, B., HOLTSCHKE, T., SCHNEEMANN, M., BACHMANN, M.F., MAK, T.W., HORAK, I., and ZINKERNAGEL, R.M. (1997). Crucial role of interferon consensus sequence binding protein, but neither of interferon regulatory factor 1 nor of nitric oxide synthesis for protection against murine listeriosis. J. Exp. Med. 185, 921-931. source
- Not checked yetcites [39] 39. HEIN, J., KEMPF, V.A., DIEBOLD, J., BUCHELER, N., PREGER, S., HORAK, I., SING, A., KRAMER, U., and AUTENRIETH, I.B. (2000). Interferon consensus sequence binding protein confers resistance against Yersinia enterocolitica . Infect. Immun. 68, 1408-1417. source
- Not checked yetcites [40] 40. GIESE, N.A., GABRIELE, L., DOHERTY, T.M., KLINMAN, D.M., TADESSE-HEATH, L., CONTURSI, C., EPSTEIN, S.L., and MORSE, H.C., 3rd (1997). Interferon (IFN) consensus sequence-binding protein, a transcription factor of the IFN regulatory factor family, regulates immune responses in vivo through control of interleukin 12 expression. J. Exp. Med. 186, 1535-1546. source
- Not checked yetcites [41] 41. SCHARTON-KERSTEN, T., CONTURSI, C., MASUMI, A., SHER, A., and OZATO, K. (1997). Interferon consensus sequence binding protein-deficient mice display impaired resistance to intracellular infection due to a primary defect in interleukin 12 p40 induction. J. Exp. Med. 186, 1523-1534. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § IMMUNODEFICIENCY OF ICSBP 2 / 2 MICE · plain
None of the sources cited for this claim have been checked yet.
In the paper
“Interferon (IFN) consensus sequence binding protein (ICSBP)/IFN regulatory factor (IRF)-8 is an IFN g -inducible transcription factor of the IRF family and regulates transcription through multiple target DNA elements, such as IFN-stimulated response element (ISRE), Ets/IRF composite element, and IFNg activation site (GAS).”
- Also stated in: § CLONING, STRUCTURE, AND EXPRESSION OF ICSBP · hedged
“ICSBP is expressed in the hematopoietic cells, including cells of the monocyte/macrophage lineage, B lymphocytes, and activated T lymphocytes, and is inducible by IFNg in these cells, suggesting its role in immune cells. (6,9-13)”
- Also stated in: § TARGET DNA ELEMENTS, INTERACTING PROTEINS, AND REGULATION OF TRANSCRIPTION · hedged
“Recent studies indicate that ICSBP can act on a wide range of target elements even beyond the IRS, such as the Ets site in IL-12 p40 promoter and the IFNg activation site (GAS). (15,34)”
What the sources say
- Not checked yetcites [6] 6. WEISZ, A., MARX, P., SHARF, R., APPELLA, E., DRIGGERS, P.H., OZATO, K., and LEVI, B.-Z. (1992). Human interferon consensus sequence binding protein is a negative regulator of enhancer elements common to interferon-inducible genes. J. Biol. Chem. 267, 25589-25596. source
- Not checked yetcites [9] 9. POLITIS, A.D., SIVO, J., DRIGGERS, P.H., OZATO, K., and VOGEL, S.N. (1992). Modulation of interferon consensus sequence binding protein mRNA in murine peritoneal macrophages. Induction by IFN-gamma and down-regulation by IFN-alpha, dexamethasone, and protein kinase inhibitors. J. Immunol. 148, 801807. source
- Not checked yetcites [10] 10. KANNO, Y., KOZAK, C.A., SCHINDLER, C., DRIGGERS, P.H., ENNIST, D.L., GLEASON, S.L., DARNELL, J.E., Jr., and OZATO, K. (1993). The genomic structure of the murine ICSBP gene reveals the presence of the gamma interferon-responsive element, to which an ISGF3 alpha subunit (or similar) molecule binds. Mol. Cell. Biol. 13, 3951-3963. source
- Not checked yetcites [11] 11. POLITIS, A.D., OZATO, K., COLIGAN, J.E., and VOGEL, S.N. (1994). Regulation of IFN-gamma-induced nuclear expression of IFN consensus sequence binding protein in murine peritoneal macrophages. J. Immunol. 152, 2270-2278. source
- Not checked yetcites [12] 12. NELSON, N., KANNO, Y., HONG, C., CONTURSI, C., FUJITA, T., FOWLKES, B.J., O'CONNELL, E., HU-LI, J., PAUL, W.E., JANKOVIC, D., SHER, A.F., COLIGAN, J.E., THORNTON, A., APPELLA, E., YANG, Y., and OZATO, K. (1996). Expression of IFN regulatory factor family proteins in lymphocytes. Induction of Stat-1 and IFN consensus sequence binding protein expression by T cell activation. J. Immunol. 156, 3711-3720. source
- Not checked yetcites [13] 13. KANTAKAMALAKUL, W., POLITIS, A.D., MARECKI, S., SULLIVAN, T., OZATO, K., FENTON, M.J., and VOGEL, S.N. (1999). Regulation of IFN consensus sequence binding protein expression in murine macrophages. J. Immunol. 162, 7417-7425. source
- Not checked yetcites [15] 15. WANG, I.M., CONTURSI, C., MASUMI, A., MA, X., TRINCHIERI, G., and OZATO, K. (2000). An IFN-gamma-inducible transcription factor, IFN consensus sequence binding protein (ICSBP), stimulates IL-12 p40 expression in macrophages. J. Immunol. 165, 271-279. source
- Not checked yetcites [34] 34. CONTURSI, C., WANG, I.M., GABRIELE, L., GADINA, M., O'SHEA, J., MORSE, H.C., 3rd, and OZATO, K. (2000). IFN consensus sequence binding protein potentiates Stat1-dependent activation of IFNgamma-responsive promoters in macrophages. Proc. Natl. Acad. Sci. USA 97, 91-96. source
- Not checked yetcites [2] 2. NGUYEN, H., HISCOTT, J., and PITHA, P.M. (1997). The growing family of interferon regulatory factors. Cytokine Growth Factor Rev. 8, 293-312. source
- Not checked yetcites [3] 3. TANIGUCHI, T., OGASAWARA, K., TAKAOKA, A., and TANAKA, N. (2001). IRF family of transcription factors as regulators of host defense. Annu. Rev. Immunol. 19, 623-655. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § CLONING, STRUCTURE, AND EXPRESSION OF ICSBP · hedged
None of the sources cited for this claim have been checked yet.
In the paper
“It also associates with PU.1 and stimulates activity of the Ets/IRF composite element (EICE), which also contains IRS and is present in the immunoglobulin (Ig) k and l , gp91 phox , scavenger receptor, toll-like receptor-4 (TLR-4), and interleukin (IL)-1 b genes. (5,23,26-30)”
What the sources say
- Not checked yetcites [5] 5. MERARO, D., HASHMUELI, S., KOREN, B., AZRIEL, A., OUMARD, A., KIRCHHOFF, S., HAUSER, H., NAGULAPALLI, S., ATCHISON, M.L., and LEVI, B.-Z. (1999). Proteinprotein and DNA-protein interactions affect the activity of lymphoid-specific IFN regulatory factors. J. Immunol. 163, 64686478. source
- Not checked yetcites [23] 23. FUJII, Y., SHIMIZU, T., KUSUMOTO, M., KYOGOKU, Y., TANIGUCHI, T., and HAKOSHIMA, T. (1999). Crystal structure of an IRF-DNA complex reveals novel DNA recognition and cooperative binding to a tandem repeat of core sequences. EMBO J. 18, 5028-5041. source
- Not checked yetcites [26] 26. BRASS, A.L., ZHU, A.Q., and SINGH, H. (1999). Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers. EMBO J. 18, 977-991. source
- Not checked yetcites [27] 27. MARECKI, S., ATCHISON, M.L., and FENTON, M.J. (1999). Differential expression and distinct functions of IFN regulatory factor 4 and IFN consensus sequence binding protein in macrophages. J. Immunol. 163, 2713-2722. source
- Not checked yetcites [28] 28. EKLUND, E.A, JALAVA, A., and KAKAR, R. (1998). PU.1, interferon regulatory factor 1, and interferon consensus sequencebinding protein cooperate to increase gp91 (phox) expression. J. Biol. Chem. 273, 13957-13965. source
- Not checked yetcites [29] 29. REHLI, M., POLTORAK, A., SCHWARZFISCHER, L., KRAUSE, S.W., ANDREESEN, R., and BEUTLER, B. (2000). PU.1 and interferon consensus sequence-binding protein regulate the myeloid expression of the human toll-like receptor 4 gene. J. Biol. Chem. 275, 9773-9781. source
- Not checked yetcites [30] 30. MARECKI, S., RIENDEAU, C.J., LIANG, M.D., and FENTON, M.J. (2001). PU.1 and multiple IFN regulatory factor proteins synergize to mediate transcriptional activation of the human IL-1beta gene. J. Immunol. 166, 6829-6838. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In addition, ICSBP 2 / 2 mice develop a chronic myelogenous leukemia (CML)-like syndrome, where a systemic expansion of granulocytes is followed by a fatal blast crisis.”
- Also stated in: § ROLE OF ICSBP IN MYELOID CELL DIFFERENTIATION · plain
“Unexpectedly, ICSBP 2 / 2 mice were found to develop a syndrome resembling CML in humans. (37)”
What the sources say
- Not checked yetcites [37] 37. HOLTSCHKE, T., LOHLER, J., KANNO, Y., FEHR, T., GIESE, N., ROSENBAUER, F., LOU, J., KNOBELOCH, K.P., GABRIELE, L., WARING, J.F., BACHMANN, M.F., ZINKERNAGEL, R.M., MORSE, H.C., 3rd, OZATO, K., and HORAK, I. (1996). Immunodeficiency and chronic myelogenous leukemia-like syndrome in mice with a targeted mutation of the ICSBP gene. Cell 87, 307-317. source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Also stated in: § ROLE OF ICSBP IN MYELOID CELL DIFFERENTIATION · plain
None of the sources cited for this claim have been checked yet.
In the paper
“ICSBP 2 / 2 mice harbor an increased number of myeloid progenitor cells, and the 2 / 2 progenitors preferentially give rise to granulocytes, although they cannot efficiently generate another descendant of the myeloid lineage, macrophages.”
- Also stated in: § Regulation of myeloid cell growth and differentiation · plain
“It was shown that adult bone marrow and fetal liver of ICSBP 2 / 2 mice harbor increased numbers of progenitor cells, which are hyperresponsive to both granulocyte-macrop hage colony-stimulating factor (GM-CSF) and granulocyte colonystimulating factor (G-CSF) in vitro , as assessed by colony-forming assay. (49)”
What the sources say
- Not checked yetcites [49] 49. SCHELLER, M., FOERSTER, J., HEYWORTH, C.M., WARING, J.F., LOHLER, J., GILMORE, G.L., SHADDUCK, R.K., DEXTER, T.M., and HORAK, I. (1999). Altered development and cytokine responses of myeloid progenitors in the absence of transcription factor, interferon consensus sequence binding protein. Blood 94, 3764-3771. source
- Not checked yetcites [54] 54. TAMURA, T., NAGAMURA-INOUE, T., SHMELTZER, Z., KUWATA, T., and OZATO, K. (2000). ICSBP directs bipotential myeloid progenitor cells to differentiate into mature macrophages. Immunity 13, 155-165. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § Regulation of myeloid cell growth and differentiation · plain
None of the sources cited for this claim have been checked yet.
In the paper
“ICSBP is expressed in the hematopoietic cells, including cells of the monocyte/macrophage lineage, B lymphocytes, and activated T lymphocytes, and is inducible by IFNg in these cells, suggesting its role in immune cells. (6,9-13)”
What the sources say
- Not checked yetcites [6] 6. WEISZ, A., MARX, P., SHARF, R., APPELLA, E., DRIGGERS, P.H., OZATO, K., and LEVI, B.-Z. (1992). Human interferon consensus sequence binding protein is a negative regulator of enhancer elements common to interferon-inducible genes. J. Biol. Chem. 267, 25589-25596. source
- Not checked yetcites [9] 9. POLITIS, A.D., SIVO, J., DRIGGERS, P.H., OZATO, K., and VOGEL, S.N. (1992). Modulation of interferon consensus sequence binding protein mRNA in murine peritoneal macrophages. Induction by IFN-gamma and down-regulation by IFN-alpha, dexamethasone, and protein kinase inhibitors. J. Immunol. 148, 801807. source
- Not checked yetcites [10] 10. KANNO, Y., KOZAK, C.A., SCHINDLER, C., DRIGGERS, P.H., ENNIST, D.L., GLEASON, S.L., DARNELL, J.E., Jr., and OZATO, K. (1993). The genomic structure of the murine ICSBP gene reveals the presence of the gamma interferon-responsive element, to which an ISGF3 alpha subunit (or similar) molecule binds. Mol. Cell. Biol. 13, 3951-3963. source
- Not checked yetcites [11] 11. POLITIS, A.D., OZATO, K., COLIGAN, J.E., and VOGEL, S.N. (1994). Regulation of IFN-gamma-induced nuclear expression of IFN consensus sequence binding protein in murine peritoneal macrophages. J. Immunol. 152, 2270-2278. source
- Not checked yetcites [12] 12. NELSON, N., KANNO, Y., HONG, C., CONTURSI, C., FUJITA, T., FOWLKES, B.J., O'CONNELL, E., HU-LI, J., PAUL, W.E., JANKOVIC, D., SHER, A.F., COLIGAN, J.E., THORNTON, A., APPELLA, E., YANG, Y., and OZATO, K. (1996). Expression of IFN regulatory factor family proteins in lymphocytes. Induction of Stat-1 and IFN consensus sequence binding protein expression by T cell activation. J. Immunol. 156, 3711-3720. source
- Not checked yetcites [13] 13. KANTAKAMALAKUL, W., POLITIS, A.D., MARECKI, S., SULLIVAN, T., OZATO, K., FENTON, M.J., and VOGEL, S.N. (1999). Regulation of IFN consensus sequence binding protein expression in murine macrophages. J. Immunol. 162, 7417-7425. source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“ICSBP interacts with IRF-1, IRF2, or IRF-4 on the ISRE and negatively regulates some IFNinducible genes, such as ISG15 , which carries a functional ISRE. (4,24,25)”
What the sources say
- Not checked yetcites [4] 4. SHARF, R., AZRIEL, A., LEJBKOWICZ, F., WINOGRAD, S.S., EHRLICH, R., and LEVI, B.-Z. (1995). Functional domain analysis of interferon consensus sequence binding protein (ICSBP) and its association with interferon regulatory factors. J. Biol. Chem. 270, 13063-13069. source
- Not checked yetcites [24] 24. BOVOLENTA, C., DRIGGERS, P.H., MARKS, M.S., MEDIN, J.A., POLITIS, A.D., VOGEL, S.N., LEVY, D.E., SAKAGUCHI, K., APPELLA, E., COLIGAN, J.E., et al. (1994). Molecular interactions between interferon consensus sequence binding protein and members of the interferon regulatory factor family. Proc. Natl. Acad. Sci. USA 91, 5046-5050. source
- Not checked yetcites [25] 25. ROSENBAUER, F., WARING, J.F., FOERSTER, J., WIETSTRUK, M., PHILIPP, D., and HORAK, I. (1999). Interferon consensus sequence binding protein and interferon regulatory factor4/Pip form a complex that represses the expression of the interferon-stimulated gene-15 in macrophages. Blood 94, 42744281. source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“ICSBP 2 / 2 mice were shown to be deficient in producing IL-12 and IFNg and were unable to mount a Th1-mediated response. (37,40,41)”
What the sources say
- Not checked yetcites [37] 37. HOLTSCHKE, T., LOHLER, J., KANNO, Y., FEHR, T., GIESE, N., ROSENBAUER, F., LOU, J., KNOBELOCH, K.P., GABRIELE, L., WARING, J.F., BACHMANN, M.F., ZINKERNAGEL, R.M., MORSE, H.C., 3rd, OZATO, K., and HORAK, I. (1996). Immunodeficiency and chronic myelogenous leukemia-like syndrome in mice with a targeted mutation of the ICSBP gene. Cell 87, 307-317. source
- Not checked yetcites [40] 40. GIESE, N.A., GABRIELE, L., DOHERTY, T.M., KLINMAN, D.M., TADESSE-HEATH, L., CONTURSI, C., EPSTEIN, S.L., and MORSE, H.C., 3rd (1997). Interferon (IFN) consensus sequence-binding protein, a transcription factor of the IFN regulatory factor family, regulates immune responses in vivo through control of interleukin 12 expression. J. Exp. Med. 186, 1535-1546. source
- Not checked yetcites [41] 41. SCHARTON-KERSTEN, T., CONTURSI, C., MASUMI, A., SHER, A., and OZATO, K. (1997). Interferon consensus sequence binding protein-deficient mice display impaired resistance to intracellular infection due to a primary defect in interleukin 12 p40 induction. J. Exp. Med. 186, 1523-1534. source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“I NTERFERON (IFN) CONSENSUS SEQUENCE BINDING (ICSBP), also designated IFN regulatory factor-8 (IRF-8), was originally cloned as a nuclear protein that binds to IFN consensus sequence (ICS) in the major histocompatibility complex (MHC) class I genes. (1)”
What the sources say
- Not checked yetcites [1] 1. DRIGGERS, P.H., ENNIST, D.L., GLEASON, S.L., MAK, W.H., MARKS, M.S., LEVI, B.Z., FLANAGAN, J.R., APPELLA, E., and OZATO, K. (1990). An interferon gamma-regulated protein that binds the interferon-inducible enhancer element of major histocompatibility complex class I genes. Proc. Natl. Acad. Sci. USA 87, 3743-3747. source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“It belongs to the family of IRF transcription factors, which includes nine mammalian members and four virally encoded homologs. (2,3)”
What the sources say
- Not checked yetcites [2] 2. NGUYEN, H., HISCOTT, J., and PITHA, P.M. (1997). The growing family of interferon regulatory factors. Cytokine Growth Factor Rev. 8, 293-312. source
- Not checked yetcites [3] 3. TANIGUCHI, T., OGASAWARA, K., TAKAOKA, A., and TANAKA, N. (2001). IRF family of transcription factors as regulators of host defense. Annu. Rev. Immunol. 19, 623-655. source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“ICSBP was shown to bind Trip15 (CSN2), which is a component of the COP9/signalosome (CSN) complex.”
- Also stated in: § PHOSPHORYLATION OF ICSBP · plain
“The CSN complex was able to phosphorylate a serine residue within the IAD of ICSBP, the residue of which phosphorylation is essential for efficient association with IRF-1. (36)”
What the sources say
- Not checked yetcites [36] 36. COHEN, H., AZRIEL, A., COHEN, T., MERARO, D., HASHMUELI, S., BECH-OTSCHIR, D., KRAFT, R., DUBIEL, W., and LEVI, B.-Z. (2000). Interaction between interferon consensus sequence-binding protein and COP9/signalosome subunit CSN2 (Trip15). A possible link between interferon regulatory factor signaling and the COP9/signalosome. J. Biol. Chem. 275, 3908139089. source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § PHOSPHORYLATION OF ICSBP · plain
In the paper
“Interactions with IRF-1/2 and PU.1 significantly enhance DNA-binding activity of ICSBP and are mediated through the IAD. (5)”
What the sources say
- Not checked yetcites [5] 5. MERARO, D., HASHMUELI, S., KOREN, B., AZRIEL, A., OUMARD, A., KIRCHHOFF, S., HAUSER, H., NAGULAPALLI, S., ATCHISON, M.L., and LEVI, B.-Z. (1999). Proteinprotein and DNA-protein interactions affect the activity of lymphoid-specific IFN regulatory factors. J. Immunol. 163, 64686478. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Studies with myeloid progenitor cells have shown that ICSBP drives their differentiation toward macrophage, whereas it inhibits granulocyte differentiation.”
- Also stated in: § Regulation of myeloid cell growth and differentiation · plain
“Transduction of a retrovirus carrying the ICSBP gene caused marked differentiation in the progenitor cells, leading to generation of mature macrophages with phagocytic activity, which coincided with the induction of DNA-binding activity specific for ISRE and EICE (Fig. 3). (54)”
What the sources say
- Not checked yetcites [54] 54. TAMURA, T., NAGAMURA-INOUE, T., SHMELTZER, Z., KUWATA, T., and OZATO, K. (2000). ICSBP directs bipotential myeloid progenitor cells to differentiate into mature macrophages. Immunity 13, 155-165. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § Regulation of myeloid cell growth and differentiation · plain
In the paper
“Although this Tyr phosphorylation negatively regulates ICSBP's own DNA binding activity, it is essential for the formation of heterodimer with IRF-1/2, and Tyr-phosphorylated ICSBP can bind target DNA only through association with IRF-1/2. (35)”
What the sources say
- Not checked yetcites [35] 35. SHARF, R., MERARO, D., AZRIEL, A., THORNTON, A.M., OZATO, K., PETRICOIN, E.F., LARNER, A.C., SCHAPER, F., HAUSER, H., and LEVI, B.-Z. (1997). Phosphorylation events modulate the ability of interferon consensus sequence binding protein to interact with interferon regulatory factors and to bind DNA. J. Biol. Chem. 272, 9785-9792. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“ICSBP has the DNAbinding domain (DBD) conserved in the IRF family at the Nterminal region and the IRF association domain (IAD) in the C-terminal region (Fig. 1). (2-5)”
What the sources say
- Not checked yetcites [2] 2. NGUYEN, H., HISCOTT, J., and PITHA, P.M. (1997). The growing family of interferon regulatory factors. Cytokine Growth Factor Rev. 8, 293-312. source
- Not checked yetcites [3] 3. TANIGUCHI, T., OGASAWARA, K., TAKAOKA, A., and TANAKA, N. (2001). IRF family of transcription factors as regulators of host defense. Annu. Rev. Immunol. 19, 623-655. source
- Not checked yetcites [4] 4. SHARF, R., AZRIEL, A., LEJBKOWICZ, F., WINOGRAD, S.S., EHRLICH, R., and LEVI, B.-Z. (1995). Functional domain analysis of interferon consensus sequence binding protein (ICSBP) and its association with interferon regulatory factors. J. Biol. Chem. 270, 13063-13069. source
- Not checked yetcites [5] 5. MERARO, D., HASHMUELI, S., KOREN, B., AZRIEL, A., OUMARD, A., KIRCHHOFF, S., HAUSER, H., NAGULAPALLI, S., ATCHISON, M.L., and LEVI, B.-Z. (1999). Proteinprotein and DNA-protein interactions affect the activity of lymphoid-specific IFN regulatory factors. J. Immunol. 163, 64686478. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These results illustrate the mechanism by which the loss of ICSBP leads to immunodeficiency and CML-like syndrome and suggest ICSBP's critical role in the development of myeloid cells.”
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Lipopolysaccharide (LPS) also induces ICSBP, albeit to a lesser degree, and synergizes with IFNg in macrophages. (13-15)”
What the sources say
- Not checked yetcites [13] 13. KANTAKAMALAKUL, W., POLITIS, A.D., MARECKI, S., SULLIVAN, T., OZATO, K., FENTON, M.J., and VOGEL, S.N. (1999). Regulation of IFN consensus sequence binding protein expression in murine macrophages. J. Immunol. 162, 7417-7425. source
- Not checked yetcites [14] 14. BARBER, S.A., FULTZ, M.J., SALKOWSKI, C.A., and VOGEL, S.N. (1995). Differential expression of interferon regulatory factor 1 (IRF-1), IRF-2, and interferon consensus sequence binding protein genes in lipopolysaccharide (LPS)-responsive and LPS-hyporesponsive macrophages. Infect. Immun. 63, 601-608. source
- Not checked yetcites [15] 15. WANG, I.M., CONTURSI, C., MASUMI, A., MA, X., TRINCHIERI, G., and OZATO, K. (2000). An IFN-gamma-inducible transcription factor, IFN consensus sequence binding protein (ICSBP), stimulates IL-12 p40 expression in macrophages. J. Immunol. 165, 271-279. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“ICSBP may play an important role in the pathogenesis of leukemia not only as an intrinsic regulator in the leukemic cells but also as an immune regulator.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“A recent study suggests that ICSBP potentiates activation of GAS in macrophages. (34)”
- Also stated in: § ICSBPretrovirus · plain
“Macrophages from ICSBP 2 / 2 mice were found to be defective in inducing some IFNg -responsive genes, such as Fc g receptor I (Fc g RI) and nitric oxide synthase (iNOS) genes. However, they were capable of activating Stat1 in response to IFNg .”
What the sources say
- Not checked yetcites [34] 34. CONTURSI, C., WANG, I.M., GABRIELE, L., GADINA, M., O'SHEA, J., MORSE, H.C., 3rd, and OZATO, K. (2000). IFN consensus sequence binding protein potentiates Stat1-dependent activation of IFNgamma-responsive promoters in macrophages. Proc. Natl. Acad. Sci. USA 97, 91-96. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § ICSBPretrovirus · plain
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These results suggest that whereas ICSBP stimulates expression of genes important for macrophage differentiation, it represses a series of genes required for granulocyte differentiation and that the two events are internally coupled through the action of ICSBP (Fig. 4).”
- Also stated in: § Regulation of myeloid cell growth and differentiation · hedged
“The dual mode of ICSBP action indicates that it plays a critical role in the lineage selection of myeloid progenitor.”
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § Regulation of myeloid cell growth and differentiation · hedged
In the paper
“It is interesting to note that ICSBP induces a zinc finger transcription factor Egr-1 that has been implicated in macrophage differentiation, (57)”
What the sources say
- Not checked yetcites [57] 57. NGUYEN, H.Q., HOFFMAN, L.B., and LIEBERMANN, D.A. - (1993). The zinc finger transcription factor Egr-1 is essential for and restricts differentiation along the macrophage lineage. Cell 72, 197-209. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, it was suggested that ICSBP regulates the proliferation and differentiation of hematopoietic cells and may act as a tumor suppressor.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Unexpectedly, ICSBP 2 / 2 mice were found to develop a syndrome resembling CML in humans. (37)”
- Also stated in: § ROLE OF ICSBP IN MYELOID CELL DIFFERENTIATION · plain
“The most significant alteration was a systemic expansion and infiltration of granulocytes (predominantly mature neutrophils), causing lymphadenopathy and hepatosplenomegaly, which was observed in essentially 100% of ICSBP 2 / 2 mice.”
What the sources say
- Not checked yetcites [37] 37. HOLTSCHKE, T., LOHLER, J., KANNO, Y., FEHR, T., GIESE, N., ROSENBAUER, F., LOU, J., KNOBELOCH, K.P., GABRIELE, L., WARING, J.F., BACHMANN, M.F., ZINKERNAGEL, R.M., MORSE, H.C., 3rd, OZATO, K., and HORAK, I. (1996). Immunodeficiency and chronic myelogenous leukemia-like syndrome in mice with a targeted mutation of the ICSBP gene. Cell 87, 307-317. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § ROLE OF ICSBP IN MYELOID CELL DIFFERENTIATION · plain
In the paper
“These progenitor cells grew in a GM-CSF-dependent manner and were capable of differentiating into mature granulocytes in response to G-CSF.”
- Also stated in: § Regulation of myeloid cell growth and differentiation · plain
“Transduction of a retrovirus carrying the ICSBP gene caused marked differentiation in the progenitor cells, leading to generation of mature macrophages with phagocytic activity, which coincided with the induction of DNA-binding activity specific for ISRE and EICE (Fig. 3). (54)”
- Also stated in: § Regulation of myeloid cell growth and differentiation · plain
“Furthermore, ICSBP inhibited G-CSF-mediated granulocyte growth and differentiation in the ICSBP 2 / 2 progenitor cells and in the 32Dcl.3 myeloid progenitor cell line. (54)”
What the sources say
- Not checked yetcites [54] 54. TAMURA, T., NAGAMURA-INOUE, T., SHMELTZER, Z., KUWATA, T., and OZATO, K. (2000). ICSBP directs bipotential myeloid progenitor cells to differentiate into mature macrophages. Immunity 13, 155-165. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § Regulation of myeloid cell growth and differentiation · plain
In the paper
“It was shown that adult bone marrow and fetal liver of ICSBP 2 / 2 mice harbor increased numbers of progenitor cells, which are hyperresponsive to both granulocyte-macrop hage colony-stimulating factor (GM-CSF) and granulocyte colonystimulating factor (G-CSF) in vitro , as assessed by colony-forming assay. (49)”
- Also stated in: § Regulation of myeloid cell growth and differentiation · boosted
“In contrast, their response to macrophage colony-stimulating factor (M-CSF) was strongly reduced, and, surprisingly, ICSBP 2 / 2 colonies formed in the presence of M-CSF were mostly granulocytes.”
What the sources say
- Not checked yetcites [49] 49. SCHELLER, M., FOERSTER, J., HEYWORTH, C.M., WARING, J.F., LOHLER, J., GILMORE, G.L., SHADDUCK, R.K., DEXTER, T.M., and HORAK, I. (1999). Altered development and cytokine responses of myeloid progenitors in the absence of transcription factor, interferon consensus sequence binding protein. Blood 94, 3764-3771. source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § Regulation of myeloid cell growth and differentiation · boosted
In the paper
“IFNa , the effective cytokine for therapy of CML, induced ICSBP expression in vivo , and the ICSBP expression correlated with pretreatment risk features and cytogenetic response to IFNa in CML. (51)”
What the sources say
- Not checked yetcites [51] 51. SCHMIDT, M., HOCHHAUS, A., NITSCHE, A., HEHLMANN, R., and NEUBAUER, A. (2001). Expression of nuclear transcription factor interferon consensus sequence binding protein in chronic myeloid leukemia correlates with pretreatment risk features and cytogenetic response to interferon-alpha. Blood 97, 3648-3650. source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Furthermore, it was shown that forced expression of ICSBP induces potent immunity against Bcr-Abl-induced leukemia in mice. (53)”
- Also stated in: § ROLE OF ICSBP IN MYELOID CELL DIFFERENTIATION · plain
“Although ectopic expression of ICSBP did not alter in vitro growth of Bcr-Abl-transformed BaF3 cells, in vivo leukemia caused by the transformed BaF3 was completely inhibited by coexpression of ICSBP.”
What the sources say
- Not checked yetcites [53] 53. DENG, M., and DALEY, G.Q. (2001). Expression of interferon consensus sequence binding protein induces potent immunity against Bcr/Abl-induced leukemia. Blood 97, 3491-3497. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § ROLE OF ICSBP IN MYELOID CELL DIFFERENTIATION · plain
In the paper
“In the mouse model with a CML-like disease induced by Bcr-Abl, ICSBP expression was also downregulated. Interestingly, the mouse disease was ameliorated by coexpression of ICSBP. (52)”
What the sources say
- Not checked yetcites [52] 52. HAO, S.X., and REN, R. (2000). Expression of interferon consensus sequence binding protein (ICSBP) is downregulated in BcrAbl-induced murine chronic myelogenous leukemia-like disease, and forced coexpression of ICSBP inhibits Bcr-Abl-induced myeloproliferative disorder. Mol. Cell. Biol. 20, 1149-1161. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“It was shown that ICSBP alone is able to activate mouse and human IL-12 p40 promoters.”
- Also stated in: § Regulation of IL-12 p40 gene by ICSBP · hedged
“Analysis of human IL-12 p40 promoter indicated that ICSBP acts through the Ets site, known to be important for activation by IFNg /LPS. (15)”
- Also stated in: § Regulation of IL-12 p40 gene by ICSBP · plain
“Although exogenous IRF-1, also shown to be necessary for IL-12 p40 gene expression, (45,46) had no effect on its own, it synergized with ICSBP.”
What the sources say
- Not checked yetcites [15] 15. WANG, I.M., CONTURSI, C., MASUMI, A., MA, X., TRINCHIERI, G., and OZATO, K. (2000). An IFN-gamma-inducible transcription factor, IFN consensus sequence binding protein (ICSBP), stimulates IL-12 p40 expression in macrophages. J. Immunol. 165, 271-279. source
- Not checked yetcites [45] 45. TAKI, S., SATO, T., OGASAWARA, K., FUKUDA, T., SATO, M., HIDA, S., SUZUKI, G., MITSUYAMA, M., SHIN, E.H., KOJIMA, S., TANIGUCHI, T., and ASANO, Y. (1997). Multistage regulation of Th1-type immune responses by the transcription factor IRF-1. Immunity 6, 673-679. source
- Not checked yetcites [46] 46. SALKOWSKI, C.A., KOPYDLOWSKI, K., BLANCO, J., CODY, M.J., McNALLY, R., and VOGEL, S.N. (1999). IL-12 is dysreg- - ulated in macrophages from IRF-1 and IRF-2 knockout mice. J. Immunol. 163, 1529-1536. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § Regulation of IL-12 p40 gene by ICSBP · hedged
None of the sources cited for this claim have been checked yet.
In the paper
“Strikingly, ICSBP 2 / 2 macrophages or cells from draining lymph nodes were severely impaired in both basal and induced expression of the IL-12 p40 gene after infection. (40,41)”
- Also stated in: § Regulation of IL-12 p40 gene by ICSBP · plain
“A similar impairment was noted for peritoneal macrophages in response to various in vitro stimuli, such as LPS, Staphylococcus aureus Cowan strain 1 (SAC), or soluble tachyzoite antigen (STAg) from T. gondii with and without IFNg pretreatment. (40,41)”
What the sources say
- Not checked yetcites [40] 40. GIESE, N.A., GABRIELE, L., DOHERTY, T.M., KLINMAN, D.M., TADESSE-HEATH, L., CONTURSI, C., EPSTEIN, S.L., and MORSE, H.C., 3rd (1997). Interferon (IFN) consensus sequence-binding protein, a transcription factor of the IFN regulatory factor family, regulates immune responses in vivo through control of interleukin 12 expression. J. Exp. Med. 186, 1535-1546. source
- Not checked yetcites [41] 41. SCHARTON-KERSTEN, T., CONTURSI, C., MASUMI, A., SHER, A., and OZATO, K. (1997). Interferon consensus sequence binding protein-deficient mice display impaired resistance to intracellular infection due to a primary defect in interleukin 12 p40 induction. J. Exp. Med. 186, 1523-1534. source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § Regulation of IL-12 p40 gene by ICSBP · plain
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It is apparent that ICSBP regulates IL-12 p40 gene activation and, as a consequence, promotes IFNg -dependent host resistance.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“IL-12 is composed of the p35 and p40 subunits, forming a heterodimer p70. (42)”
What the sources say
- Not checked yetcites [42] 42. TRINCHIERI, G. (1998). Interleukin-12: a cytokine at the interface of inflammation and immunity. Adv. Immunol. 70, 83-243. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“ICSBP may act upstream of Egr-1, and once Egr-1 is induced by ICSBP, it may generate a secondary cascade of gene expression emanating from Egr-1.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It directs them to differentiate into macrophages and facilitates their functional maturation while it inhibits growth and differentiation of granulocytes.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“ICSBP also interacts with IRF-1 and IRF-2 and antagonizes IRF-1 activation of promoters through the standard ISRE.”
What the sources say
- Not checked yetcites [15] 15. WANG, I.M., CONTURSI, C., MASUMI, A., MA, X., TRINCHIERI, G., and OZATO, K. (2000). An IFN-gamma-inducible transcription factor, IFN consensus sequence binding protein (ICSBP), stimulates IL-12 p40 expression in macrophages. J. Immunol. 165, 271-279. source
- Not checked yetcites [28] 28. EKLUND, E.A, JALAVA, A., and KAKAR, R. (1998). PU.1, interferon regulatory factor 1, and interferon consensus sequencebinding protein cooperate to increase gp91 (phox) expression. J. Biol. Chem. 273, 13957-13965. source
- Not checked yetcites [30] 30. MARECKI, S., RIENDEAU, C.J., LIANG, M.D., and FENTON, M.J. (2001). PU.1 and multiple IFN regulatory factor proteins synergize to mediate transcriptional activation of the human IL-1beta gene. J. Immunol. 166, 6829-6838. source
- Not checked yetcites [48] 48. EKLUND, E.A., and KAKAR, R. (1999). Recruitment of CREBbinding protein by PU.1, IFN-regulatory factor-1, and the IFN consensus sequence-binding protein is necessary for IFN-gammainduced p67 phox and gp91 phox expression. J. Immunol. 163, 60956105. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“in light of well-known anti-oncogenic and proapoptotic functions of IRF1 and the oncogenic potential of IRF-2, (61)”
What the sources say
- Not checked yetcites [61] 61. TANAKA, N., and TANIGUCHI, T. (2000). The interferon regulatory factors and oncogenesis. Semin. Cancer Biol. 10, 73-81. source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Its expression profoundly affects various disease processes ranging from infections to leukemia.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It directs them to differentiate into macrophages and facilitates their functional maturation while it inhibits growth and differentiation of granulocytes.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In conclusion, ICSBP is an IRF member dedicated to the growth and differentiation of myeloid cells and functional activation of macrophages.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“in light of well-known anti-oncogenic and proapoptotic functions of IRF1 and the oncogenic potential of IRF-2, (61)”
What the sources say
- Not checked yetcites [61] 61. TANAKA, N., and TANIGUCHI, T. (2000). The interferon regulatory factors and oncogenesis. Semin. Cancer Biol. 10, 73-81. source
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
46 of 46
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Although the majority of IRF family members are expressed broadly in many cell types, ICSBP and another member, Pip (IRF-4), are expressed only in the immune system (4, 12, 49).”
From Gamma Interferon Triggers Interaction between ICSBP (IRF-8) and TEL, Recruiting the Histone Deacetylase HDAC3 to the Interferon-Responsive Element (2002) · cites this paper as [49]
Citations
Cites
Darnell, J. E., Kerr, L. M., & Stark, G. R. (1994) · Science · doi:10.1126/science.8197455 · Cited by 6,080
HOW CELLS RESPOND TO INTERFERONS
Stark, G. R., Kerr, I. M., Williams, B. R. G., Silverman, R. H., & Schreiber, R. D. (1998) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.67.1.227 · Cited by 3,932
IRF Family of Transcription Factors as Regulators of Host Defense
Taniguchi, T., Ogasawara, K., Takaoka, A., & Tanaka, N. (2001) · Annual Review of Immunology · doi:10.1146/annurev.immunol.19.1.623 · Cited by 1,658
Interleukin-12: A Cytokine at the Interface of Inflammation and Immunity
Trinchieri, G. (1998) · Advances in Immunology · doi:10.1016/s0065-2776(08)60387-9 · Cited by 760
Transcription Factors, Normal Myeloid Development, and Leukemia
Tenen, D. G., Hromas, R., Licht, J. D., & Zhang, D.-E. (1997) · Blood · doi:10.1182/blood.v90.2.489 · Cited by 735
Holtschke, T., Löhler, J., Kanno, Y., Fehr, T., Giese, N., Rosenbauer, F., Lou, J., Knobeloch, K.-P., Gabriele, L., Waring, J. F., et al. (1996) · Cell · doi:10.1016/s0092-8674(00)81348-3 · Cited by 644
Self-citationRequirement for the Transcription Factor LSIRF/IRF4 for Mature B and T Lymphocyte Function
Mittrücker, H.-W., Matsuyama, T., Grossman, A., Kündig, T. M., Potter, J., Shahinian, A., Wakeham, A., Patterson, B., Ohashi, P. S., & Mak, T. W. (1997) · Science · doi:10.1126/science.275.5299.540 · Cited by 583
The growing family of interferon regulatory factors
Nguyen, H., Hiscott, J., & Pitha, P. M. (1997) · Cytokine & Growth Factor Reviews · doi:10.1016/s1359-6101(97)00019-1 · Cited by 480
Pip, a novel IRF family member, is a lymphoid-specific, PU.1-dependent transcriptional activator.
Eisenbeis, C. F., Singh, H., & Storb, U. (1995) · Genes & Development · doi:10.1101/gad.9.11.1377 · Cited by 447
Schiavoni, G., Mattei, F., Sestili, P., Borghi, P., Venditti, M., Morse, H. C., Belardelli, F., & Gabriele, L. (2002) · The Journal of Experimental Medicine · doi:10.1084/jem.20021263 · Cited by 423
Research works printed but not linked: 1
- LI W., 1999, Invest. Ophthalmol. Vis. Sci., 40, 976
Cited by
Sorted by citations
Plasmacytoid dendritic cells in immunity
Colonna, M., Trinchieri, G., & Liu, Y. (2004) · Nature Immunology · doi:10.1038/ni1141 · Cited by 1,659
IPC: Professional Type 1 Interferon-Producing Cells and Plasmacytoid Dendritic Cell Precursors
Liu, Y.-J. (2004) · Annual Review of Immunology · doi:10.1146/annurev.immunol.23.021704.115633 · Cited by 1,618
The IRF Family Transcription Factors in Immunity and Oncogenesis
Tamura, T., Yanai, H., Savitsky, D., & Taniguchi, T. (2008) · Annual Review of Immunology · doi:10.1146/annurev.immunol.26.021607.090400 · Cited by 1,259
Self-citationPietras, E. M., Reynaud, D., Kang, Y.-A., Carlin, D., Calero-Nieto, F. J., Leavitt, A. D., Stuart, J. M., Göttgens, B., & Passegué, E. (2015) · Cell stem cell · doi:10.1016/j.stem.2015.05.003 · Cited by 723
Re(de)fining the dendritic cell lineage
Satpathy, A. T., Wu, X., Albring, J. C., & MURPHY, K. M. M. (2012) · Nature Immunology · doi:10.1038/ni.2467 · Cited by 470
Metadata
- Authors
- Tamura, T., & Ozato, K.
- Affiliations
- National Institutes of Health (US)
- Venue
- Journal of Interferon & Cytokine Research
- Publisher
- SAGE Publications
- Published
- 2002-01
- Volume
- 22
- Issue
- 1
- Pages
- 145-152
- ISSN
- 1079-9907 (ISSN-L)
- 1557-7465
- OpenAlex
- W160560928
- Semantic Scholar
- 6497a15c5667a6e90a4e65ae79472ef8ed2cfa77
- Cited by
- 183
- References
- 72
- Citations by year
- 2025: 2 · 2024: 3 · 2023: 4 · 2022: 6 · 2021: 4 · 2020: 3 · 2019: 7 · 2018: 3 · 2017: 12 · 2016: 6 · 2015: 6 · 2014: 13 · 2013: 7 · 2012: 7
- FWCI
- 1.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Interferon & Cytokine Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
- Keywords
- interferon regulatory factors, myeloid cell development, macrophage differentiation, granulocytic differentiation, myeloid progenitor cells, immunodeficiency, apoptosis resistance
- MeSH terms
- Interferon Regulatory Factor-8, Animals, Cell Differentiation, Gene Expression Regulation, Humans, Phosphorylation, Repressor Proteins, Transcription Factors, Transcription, Genetic, Trans-Activators, Consensus Sequence, Apoptosis, Mice, Knockout, Myeloid Cells, Interferon Regulatory Factors, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-08, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-08 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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