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.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
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.
- 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 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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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
“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.
- 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. 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.
- 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
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.
- 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 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.
- 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 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.
- 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
“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.
- 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
“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.
- 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.
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.
- 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: § 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.
- 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
“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.
- 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
“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.
- 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
“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.
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
Items 101–183 of 183
Alter-Koltunoff, M., Ehrlich, S., Dror, N., Azriel, A., Eilers, M., Häuser, H., Bowen, H., Barton, C. H., Tamura, T., Ozato, K., et al. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m307954200 · Cited by 42
Self-citationSung, J. J. �., Park, S.-Y., Kim, J. H., Kang, H. G., Yoon, J.-H., Na, Y. S., Kim, Y.-N., & Park, B.-K. (2014) · Cell Death and Disease · doi:10.1038/cddis.2014.189 · Cited by 39
Interferon regulatory factor 8 protects against cerebral ischaemic‐reperfusion injury
Xiang, M., Wang, L., Guo, S., Lu, Y., Lei, H. C., Jiang, D., Zhang, Y., Liu, Y., Zhou, Y., Zhang, X., et al. (2014) · Journal of Neurochemistry · doi:10.1111/jnc.12682 · Cited by 39
Zhang, Q., Zhang, L., Li, L., Wang, Z., Ying, J., Fan, Y., Xu, B., Wang, L., Liu, Q., Chen, G., et al. (2014) · Cancer Letters · doi:10.1016/j.canlet.2014.07.040 · Cited by 38
Interferons and Interferon Regulatory Factors in Malaria
Gun, S. Y., Claser, C., Tan, K. S. W., & Rénia, L. (2014) · Mediators of Inflammation · doi:10.1155/2014/243713 · Cited by 38
Cooperation between deficiencies of IRF-4 and IRF-8 promotes both myeloid and lymphoid tumorigenesis
Jo, S., Schatz, J. H., Acquaviva, J., Singh, H., & Ren, R. (2010) · Blood · doi:10.1182/blood-2009-07-234559 · Cited by 37
Martı́nez, A., Pittaluga, S., Rudelius, M., DAVIES-HILL, T. M., Sebasigari, D., Fountaine, T. J., Hewitt, S. M., Jaffe, E. S., & Raffeld, M. A. (2008) · The American Journal of Surgical Pathology · doi:10.1097/pas.0b013e318166f46a · Cited by 38
Wu, H., Yan, L., Shi, G., Du, S., Wang, X., Ye, W., Zhang, Z., Chu, Y., Ma, S., Wang, D., et al. (2022) · Hepatology · doi:10.1002/hep.32316 · Cited by 38
Ivashkiv, L. B., Zhao, B., Park‐Min, K., & Takami, M. (2011) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2011.06217.x · Cited by 35
Thumbigere‐Math, V., Foster, B. L., Bachu, M., Yoshii, H., Brooks, S. R., Coulter, A. M., Chavez, M. B., Togi, S., Neely, A. L., Deng, Z., et al. (2019) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.3690 · Cited by 33
Self-citationMysterious Origin of Plasmacytoid Dendritic Cell Precursors
Wang, Y., & Liu, Y. (2004) · Immunity · doi:10.1016/j.immuni.2004.07.003 · Cited by 34
Saleem, S. J., & Conrad, D. H. (2011) · International Immunopharmacology · doi:10.1016/j.intimp.2011.03.010 · Cited by 33
Luo, X., Xiong, X., Shao, Q., Xiang, T., Li, L., Yin, X., Li, X., Tao, Q., & Ren, G. (2017) · Oncotarget · doi:10.18632/oncotarget.16511 · Cited by 32
The Innate Antiviral Response: New Insights Into A Continuing Story
Paun, A., & Pitha, P. M. (2006) · Advances in virus research · doi:10.1016/s0065-3527(06)69001-5 · Cited by 31
Horiuchi, M., Itoh, A., Pleasure, D., Ozato, K., & Itoh, T. (2011) · Journal of Neuroinflammation · doi:10.1186/1742-2094-8-8 · Cited by 30
Self-citationHu, G., Chen, X., Gong, Q., Liu, Q., Zhang, S., & Dong, X. (2013) · Fish & Shellfish Immunology · doi:10.1016/j.fsi.2013.06.016 · Cited by 30
Fragale, A., Stellacci, E., Ilari, R., Remoli, A. L., Lanciotti, A., Perrotti, E., Shytaj, I., Orsatti, R., Lawrence, H. R., Lawrence, N. J., et al. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1000918 · Cited by 27
Self-citationIFN regulatory factor–8 expression in macrophages governs an antimetastatic program
Twum, D. Y. F., Colligan, S. H., Hoffend, N. C., Katsuta, E., Gomez, E. C., Hensen, M. L., Seshadri, M., Nemeth, M. J., & Abrams, S. I. (2019) · JCI Insight · doi:10.1172/jci.insight.124267 · Cited by 28
A novel role for interferon regulatory factor 1 (IRF1) in regulation of bone metabolism
Salem, S., Gao, C., Li, A., Wang, H., Nguyen-Yamamoto, L., Goltzman, D., Henderson, J., & Gros, P. (2014) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.12327 · Cited by 28
Couch, A. C. M., Solomon, S., Duarte, R. R. R., Marrocu, A., Sun, Y., Sichlinger, L., Matulevičiūtė, R., Polit, L. D., Hanger, B., Brown, A. M., et al. (2023) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2023.02.007 · Cited by 28
Yen, J.-H. J., Kong, W., Hooper, K. M., Emig, F. A., Rahbari, K. M., Kuo, P., Scofield, B. A., & Ganea, D. (2015) · Journal of Leukocyte Biology · doi:10.1189/jlb.3hi0914-453r · Cited by 28
Mattei, F., Schiavoni, G., Borghi, P., Venditti, M., Canini, I., Sestili, P., Pietraforte, I., Morse, H. C., Ramoni, C., Belardelli, F., et al. (2006) · Blood · doi:10.1182/blood-2005-11-4490 · Cited by 28
Chen, M., Wu, M., Hu, X., Yang, J., Han, R., Ma, Y., Zhang, X., Yuan, Y., Liu, R., Jiang, G., et al. (2019) · Clinical Rheumatology · doi:10.1007/s10067-019-04505-5 · Cited by 27
TGF-β1-induced transcription factor networks in Langerhans cell development and maintenance
Zhang, X., Gu, J., Yu, F.-S., Zhou, L., & Mi, Q. (2016) · Allergy · doi:10.1111/all.12871 · Cited by 25
Relevance of Interferon Regulatory Factor-8 Expression in Myeloid–Tumor Interactions
Abrams, S. I., Netherby, C. S., Twum, D. Y. F., & Messmer, M. N. (2016) · Journal of Interferon & Cytokine Research · doi:10.1089/jir.2015.0174 · Cited by 24
Immune gene discovery by expressed sequence tag analysis of spleen in the duck (Anas platyrhynchos)
Xia, J., Radford, C., GUO, X., & Magor, K. E. (2006) · Developmental & Comparative Immunology · doi:10.1016/j.dci.2006.06.005 · Cited by 24
Enhanced osteoclastogenesis in patients with MSMD due to impaired response to IFN-γ
Tsumura, M., Miki, M., Mizoguchi, Y., Hirata, O., Nishimura, S., Tamaura, M., Kagawa, R., Hayakawa, S., Kobayashi, M., & Okada, S. (2021) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2021.05.018 · Cited by 24
Zhang, J., Liu, C., Zhao, S., Guo, S., & Shen, B. (2017) · Developmental & Comparative Immunology · doi:10.1016/j.dci.2017.10.013 · Cited by 23
Interferon regulatory factor 8 governs myeloid cell development
Xia, X., Wang, W., Yin, K., & Wang, S. (2020) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2020.03.003 · Cited by 23
Tourkova, I. L., Shurin, G. V., Ferrone, S., & Shurin, M. R. (2008) · Cancer Immunology Immunotherapy · doi:10.1007/s00262-008-0579-1 · Cited by 23
Mutational Analysis of Human Thioredoxin Reductase 1
Ma, X., Hu, J., Lindner, D. J., & Kalvakolanu, D. V. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m202286200 · Cited by 22
Das, A., Wang, X., Kang, J. M., Coulter, A. M., Shetty, A. C., Bachu, M., Brooks, S. R., Dell’Orso, S., Foster, B. L., Fan, X., et al. (2020) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.4165 · Cited by 19
Self-citationJu, X., Ruau, D., Jäntti, P., Seré, K., Becker, C., Wiercinska, E., Bartz, C., Erdmann, B., Dooley, S., & Zenke, M. (2007) · European Journal of Immunology · doi:10.1002/eji.200636504 · Cited by 20
Matejuk, A., Dwyer, J. M., Hopke, C., Vandenbark, A. A., & Offner, H. (2003) · PubMed · Cited by 19
Viglianti, G. A., Planelles, V., & Hanley, T. M. (2021) · Journal of Virology · doi:10.1128/jvi.02141-20 · Cited by 18
De, G., Chen, A., Zhao, Q., Xie, R., Wang, C., Li, M., Zhao, H., Gu, X., McCarl, L. H., Zhang, F., et al. (2021) · Pharmacological Research · doi:10.1016/j.phrs.2021.105617 · Cited by 18
A multi-functional role of interferon regulatory factor-8 in solid tumor and myeloid cell biology
Abrams, S. I. (2009) · Immunologic Research · doi:10.1007/s12026-009-8125-6 · Cited by 17
Host Immunosurveillance Controls Tumor Growth via IFN Regulatory Factor-8–Dependent Mechanisms
Greeneltch, K. M., Schneider, M., Steinberg, S. M., Liewehr, D. J., Stewart, T. J., Liu, K., & Abrams, S. I. (2007) · Cancer Research · doi:10.1158/0008-5472.can-07-1228 · Cited by 19
Punturieri, A., Copper, P., Polak, T., Christensen, P. J., & Curtis, J. L. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.177.1.673 · Cited by 17
Ebong, S., Chepelinsky, A. B., Robinson, M. L., Zhao, H., Yu, C., & Egwuagu, C. E. (2004) · PubMed · Cited by 17
Retinoic acid-induced protein ISGylation is dependent on interferon signal transduction
Dao, C. T., Luo, J.-K., & Zhang, D. (2006) · Blood Cells Molecules and Diseases · doi:10.1016/j.bcmd.2006.02.005 · Cited by 18
Down-regulation of Irf8 by Lyz2-cre/loxP accelerates osteoclast differentiation in vitro
Saito, E., Suzuki, D., Kurotaki, D., Mochizuki, A., Manome, Y., Suzawa, T., Toyoshima, Y., Ichikawa, T., Funatsu, T., Inoue, T., et al. (2016) · Cytotechnology · doi:10.1007/s10616-016-0013-z · Cited by 16
Self-citationXu, J., Deng, X., Demetriou, A. A., Farkas, D. L., Hui, T., & Wang, C. (2008) · Stem Cells and Development · doi:10.1089/scd.2007.0094 · Cited by 16
Qiu, Y., Yu, H., Zhu, Y., Ye, Z., Deng, J., Su, W., Cao, Q., Yuan, G., Kijlstra, A., & Yang, P. (2017) · Scientific Reports · doi:10.1038/s41598-017-01249-7 · Cited by 15
Li, Y., Zhang, T., Zhang, X., Wang, G., Wang, Y., & Zhang, Z. (2017) · Cell Stress and Chaperones · doi:10.1007/s12192-017-0842-5 · Cited by 15
Gurevich, R. M., Rosten, P., Schwieger, M., Stocking, C., & Humphries, R. K. (2006) · Experimental Hematology · doi:10.1016/j.exphem.2006.04.020 · Cited by 15
A Novel Transactivating Factor That Regulates Interferon-γ-dependent Gene Expression
Hu, J., Meng, Q., Roy, S. K., Raha, A., Hu, J., Zhang, J., Hashimoto, K., & Kalvakolanu, D. V. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m202679200 · Cited by 15
The Dr. Jekyll and Mr. Hyde complexity of the macrophage response in disease
Twum, D. Y. F., Burkard-Mandel, L. E., & Abrams, S. I. (2017) · Journal of Leukocyte Biology · doi:10.1189/jlb.4mr1116-479r · Cited by 13
Tinguely, M., Thies, S., Frigerio, S., Reineke, T., Korol, D., & Zimmermann, D. R. (2013) · Leukemia & lymphoma/Leukemia and lymphoma · doi:10.3109/10428194.2013.793324 · Cited by 13
Positive histone marks are associated with active transcription from a methylated ICSBP/IRF8 gene
Tshuikina, M., Nilsson, K., & Oberg, F. G. (2008) · Gene · doi:10.1016/j.gene.2007.12.013 · Cited by 12
IRF-4 Suppresses BCR/ABL Transformation of Myeloid Cells in a DNA Binding-independent Manner
Jo, S., & Ren, R. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.289728 · Cited by 11
Qiu, Y., Zhu, Y., Yu, H., Yi, S., Su, W., Cao, Q., Yuan, G., Kijlstra, A., & Yang, P. (2017) · Oncotarget · doi:10.18632/oncotarget.17235 · Cited by 11
Cai, M., & Chen, N. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.817069 · Cited by 10
An intuitionistic approach to scoring DNA sequences against transcription factor binding site motifs
García-Alcalde, F., Blanco, A. J., & Shepherd, A. J. (2010) · BMC Bioinformatics · doi:10.1186/1471-2105-11-551 · Cited by 10
Murine IRF8 Mutation Offers New Insight into Osteoclast and Root Resorption
Das, A., Yesupatham, S. K., Allison, D., Tanwar, H., Gnanasekaran, J., Kear, B. D., Wang, X., Wang, S., Zachariadou, C., Abbasi, Y., et al. (2024) · Journal of Dental Research · doi:10.1177/00220345231222173 · Cited by 9
Self-citationICSBP promoter methylation in myelodysplastic syndromes and acute myeloid leukaemia
Otto, N., Manukjan, G., Göhring, G., Hofmann, W. A., Scherer, R., Luna, J., Lehmann, U., Ganser, A., Welte, K., Schlegelberger, B., et al. (2011) · Leukemia · doi:10.1038/leu.2011.61 · Cited by 9
Dobbin, E., Graham, C., Freeburn, R. W., Unwin, R. D., Griffiths, J. R., Pierce, A., Whetton, A. D., & Wheadon, H. (2010) · Stem Cell Research · doi:10.1016/j.scr.2010.08.001 · Cited by 9
Zhang, K., Lv, D., & Li, R. (2019) · Virology · doi:10.1016/j.virol.2019.11.011 · Cited by 9
Ma, S. L., Sørensen, A. B., Kunder, S., Sørensen, K. D., Quintanilla‐Martínez, L., Morris, D. W., Schmidt, J., & Pedersen, F. S. (2006) · Virology · doi:10.1016/j.virol.2006.05.006 · Cited by 8
Singh, K., Gollapudi, S., Mittal, S., Small, C., Kumar, J., & Ohgami, R. S. (2021) · Diagnostics · doi:10.3390/diagnostics11040600 · Cited by 5
Liu, Y., He, Y., Cao, J., Lu, H., Zou, R., Zuo, Z., Li, R., Zhang, Y., & Sun, J. (2023) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2023.127138 · Cited by 5
ICSBP-induced PD-L1 enhances osteosarcoma cell growth
Sung, J. Y., Kim, J. H., Kang, H. G., Park, J. W., Park, S.-Y., Park, B.-K., & Kim, Y.-N. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.918216 · Cited by 5
Ham, H., Isham, C. R., Ristagno, E. H., Correia, C., Ennis, S. M., Kandasamy, R. K., Garapati, K., Zhang, C., Kohlhagen, M., Akha, E. S., et al. (2025) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2024.11.041 · Cited by 4
Künzi, M. S., & Pitha, P. M. (2005) · Humana Press eBooks · doi:10.1385/1-59259-939-7:025 · Cited by 7
Interferon regulatory factor 8 induces intrinsic functional changes in mature neutrophils
Polmann, L., Grimm, J. C., Roth, J., & Barczyk‐Kahlert, K. (2025) · Journal of Leukocyte Biology · doi:10.1093/jleuko/qiaf078 · Cited by 2
D’Antoni, M. L., Kallianpur, K. J., Premeaux, T. A., Corley, M. J., Fujita, T., Laws, E. I., Ogata-Arakaki, D., Chow, D. C., Khadka, V. S., Shikuma, C. M., et al. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.02789 · Cited by 2
Hanley, T. M., Planelles, V., & Viglianti, G. A. (2019) · Journal of Virus Eradication · doi:10.1016/s2055-6640(20)30090-x · Cited by 2
Li, H., Li, P., Li, S., Zhang, X., Xinru, D. O. N. G., Yang, M., & Weigan, S. (2023) · Journal of Zhejiang University (Medical Sciences) · doi:10.3724/zdxbyxb-2022-0672 · Cited by 1
Couch, A. C. M., Solomon, S., Marrocu, A., Duarte, R. R. R., Sun, Y., Sichlinger, L., Matulevičiūtė, R., Polit, L. D., Hanger, B., Kordasti, S. Y., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.08.05.502958 · Cited by 1
Chistiakov, D. A., Chernisheva, A., Savostyanov, K. V., Turakulov, R. I., Кураева, Т. Л., Dedov, I. I., & Nosikov, V. V. (2005) · PubMed · Cited by 1
pDC: From Plasmacytoid Dendritic Cell Precursorsto Professional Type 1 Interferon‐producing Cells
Liu, Y., Kanzler, H., Wang, Y., Wang, Y., Gilliet, M. F., Cao, W., & Ito, T. (2006) · Wiley eBooks · doi:10.1002/9783527619696.ch13
WILMS’ TUMOUR GENE 1 PROTEIN (WT1) – AN EFFECTOR IN LEUKEMOGENESIS?
Vidovic, K. (2010) · Lund University Publications (Lund University)
Aberrant Transcription Factors in AML
Friedman, A. D. (2007) · Humana Press eBooks · doi:10.1007/978-1-59745-322-6_2
Expression and activation of STAT and IRF family transcription factors in mononuclear leukocytes
Lehtonen, A. (2005) · Työväentutkimus Vuosikirja
Fuzzy technology for gene ontology and transcription factor binding sites
Alcalde, F. G. (2011) · Institutional Repository of the University of Granada (University of Granada)
Vidovic, K. (2010)
The role of interferon regulatory factors in LGTV infection
Zegenhagen, L. (2017) · Digitale Bibliothek Braunschweig (Verbundzentrale Göttingen (VZG)) · doi:10.24355/dbbs.084-201701181242-0
Sun, T. (2017) · TSpace (University of Toronto)
Das, A., Yesupatham, S. K., Allison, D. L., Tanwar, H., Gnanasekaran, J., Kear, B. D., Wang, X., Wang, S., Zachariadou, C., Abbasi, Y., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.04.23.537931
Self-citationImmature functional development of lumbar locomotor networks in adult Irf8−/− mice
Yazawa, I., Yoshida, Y., Yoshimi, R., & Ozato, K. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1234215
Self-citationEpigenetic regulation of gene transcription in hematopoietic tumors.
Tshuikina, M. (2008) · KTH Publication Database DiVA (KTH Royal Institute of Technology)
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.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
