The DOI matches its Crossref record; 73 of the 74 references it cites were found in a registry or an index.
Regulation of Apoptosis in Myeloid Cells by Interferon Consensus Sequence–Binding Protein
Open accessAbstract
Mice with a null mutation of the gene encoding interferon consensus sequence–binding protein (ICSBP) develop a disease with marked expansion of granulocytes and macrophages that frequently progresses to a fatal blast crisis, thus resembling human chronic myelogenous leukemia (CML). One important feature of CML is decreased responsiveness of myeloid cells to apoptotic stimuli. Here we show that myeloid cells from mice deficient in ICSBP exhibit reduced spontaneous apoptosis and a significant decrease in sensitivity to apoptosis induced by DNA damage. In contrast, apoptosis in thymocytes from ICSBP-deficient mice is unaffected. We also show that overexpression of ICSBP in the human U937 monocytic cell line enhances the rate of spontaneous apoptosis and the sensitivity to apoptosis induced by etoposide, lipopolysaccharide plus ATP, or rapamycin. Programmed cell death induced by etoposide was specifically blocked by peptides inhibitory for the caspase-1 or caspase-3 subfamilies of caspases. Studies of proapoptotic genes showed that cells overexpressing ICSBP have enhanced expression of caspase-3 precursor protein. In addition, analyses of antiapoptotic genes showed that overexpression of ICSBP results in decreased expression of Bcl-XL. These data suggest that ICSBP modulates survival of myeloid cells by regulating expression of apoptosis-related genes.
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“Myeloid cells (Gr1 1 as well as Mac1 1 cells) from ICSBP 2 / 2 were shown to exhibit reduced spontaneous apoptosis.”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [56]
In the citing paper
“Programmed cell death induced by etoposide was specifically blocked by peptides inhibitory for the caspase-1 or caspase-3 subfamilies of caspases.”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [56]
In the citing paper
“Cells overexpressing ICSBP had enhanced expression of caspase-3 precursor protein and decreased expression of Bcl-X(L).”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [56]
In the citing 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.”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [56]
In the citing 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.”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [56]
In the citing paper
“Further, in ICSBP 2 / 2 cells, there was a significant decrease in the sensitivity to apoptosis induced by DNA damage. (56)”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [56]
In the citing paper
“Cells overexpressing ICSBP had enhanced expression of caspase-3 precursor protein and decreased expression of Bcl-X(L).”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [56]
In the citing paper
“In contrast, apoptosis in ICSBP 2 / 2 thymocytes was unaffected.”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [56]
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Citations
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1 of the 74 references couldn’t be matched to a known paper.
Research works printed but not linked: 1
- Sambrook, 1989, Molecular Cloning
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Items 101–114 of 114
Wang, Y., Wang, X., Jiang, J., Li, C., & Shao, Y. (2026) · Fish & Shellfish Immunology · doi:10.1016/j.fsi.2026.111292 · Cited by 3
Molecular Biology and Cytogenetics of Chronic Myeloid Leukemia
Quintás‐Cardama, A., Kantarjian, H. M., & Cortes, J. E. (2012) · Springer eBooks · doi:10.1007/978-1-4614-3764-2_4 · Cited by 3
Molecular Biology and Cytogenetics of Chronic Myeloid Leukemia
Konopleva, M. Y., Quintás‐Cardama, A., Kantarjian, H. M., & Cortes, J. E. (2017) · Springer eBooks · doi:10.1007/978-3-319-64263-5_4 · Cited by 3
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Mayadas, T. N. (2003) · Springer eBooks · doi:10.1007/978-2-8178-0761-4_13 · Cited by 2
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Lundán, T. (2008) · Työväentutkimus Vuosikirja · Cited by 1
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Emert‐Sedlak, L. A. (2005) · D-Scholarship@Pitt (University of Pittsburgh)
WILMS’ TUMOUR GENE 1 PROTEIN (WT1) – AN EFFECTOR IN LEUKEMOGENESIS?
Vidovic, K. (2010) · Lund University Publications (Lund University)
MOLECULAR AND FUNCTIONAL STUDIES OF THE BCR/ABL1 FUSION GENE
Håkansson, P. (2006)
Zhang, H. (2012) · Digital Commons-TMC (Texas Medical Center)
Vidovic, K. (2010)
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Brauner, S. (2013)
Epigenetic regulation of gene transcription in hematopoietic tumors.
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Metadata
- Authors
- Gabriele, L., Phung, J., Fukumoto, J., Segal, D., Wang, I.-M., Giannakakou, P., Giese, N. A., Ozato, K., & Morse, H. C.
- Affiliations
- National Institute of Allergy and Infectious Diseases (US)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (US)
- National Institutes of Health (US)
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 1999-08-02
- Volume
- 190
- Issue
- 3
- Pages
- 411-422
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2195590
- OpenAlex
- W2115970169
- Cited by
- 114
- References
- 74
- Citations by year
- 2026: 1 · 2025: 2 · 2023: 2 · 2022: 2 · 2021: 2 · 2020: 1 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 6 · 2014: 6 · 2013: 7 · 2012: 5
- FWCI
- 2.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Minerva Access (University of Melbourne) (submittedVersion, cc-by-nc-sa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Keywords
- IRF8, apoptosis, myeloid cells, chronic myeloid leukemia, spontaneous apoptosis, DNA damage-induced apoptosis, caspase-3, caspase-1, Bcl-xL, anti-apoptotic genes, pro-apoptotic genes, etoposide, rapamycin, lipopolysaccharide, monocytic cells, cell survival
- MeSH terms
- Interferon Regulatory Factor-8, Amino Acid Chloromethyl Ketones, Animals, Bone Marrow Cells, Cells, Cultured, Etoposide, Gene Expression Regulation, Hematopoietic Stem Cells, Humans, Interferons, Lymph Nodes, Recombinant Proteins, Repressor Proteins, Spleen, Cysteine Proteinase Inhibitors, Consensus Sequence, Apoptosis, Mice, Knockout, Proto-Oncogene Proteins c-bcl-2, Caspases, U937 Cells, Interferon Regulatory Factors, bcl-X Protein, Mice
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