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Article: DNA damage-induced apoptosis and ice gene induction in mitogenically activated T lymphocytes require IRF-1

TitleDNA damage-induced apoptosis and ice gene induction in mitogenically activated T lymphocytes require IRF-1
Authors
Issue Date1997
Citation
Leukemia, 1997, v. 11, n. SUPPL. 3, p. 439-440 How to Cite?
AbstractLymphocytes are highly sensitive to DNA damage-induced apoptosis. In thymocytes, the tumor suppressor p53 has been shown to be required for this type of apoptosis. However an as yet unknown, p53-independent pathway(s) appears to mediate the same event in mitogenically activated mature T lymphocytes. By using mice with a null mutation in the IRF-1 gene, we revealed that DNA damage-induced apoptosis in the latter cell type is dependent on the anti-oncogenic transcription factor interferon regulatory factor-1 (IRF-1). Thus two different anti-oncogenic transcription factors, p53 and IRF-1, are required for distinct apoptotic pathways in T lymphocytes. Furthermore, we found that mitogen induction of the interleukin-1β-converting enzyme (Ice) gene, a mammalian homolog of the Caenorhabditis elegans cell death gene ced-3, is also IRF-1-dependent. An IRF-1 binding sequence was identified in the 5′ flanking region of the Ice gene. In addition, ectopic overexpression of IRF-1 results in the activation of the endogenous Ice gene and enhances the sensitivity of cells to radiation-induced apoptosis. Thus, induction of Ice gene may be involved in IRF-1 dependent DNA damage-induced apoptosis in activated mature T lymphocytes.
Persistent Identifierhttp://hdl.handle.net/10722/291398
ISSN
2023 Impact Factor: 12.8
2023 SCImago Journal Rankings: 3.662

 

DC FieldValueLanguage
dc.contributor.authorTamura, Tomohiko-
dc.contributor.authorIshihara, Masahiro-
dc.contributor.authorLamphier, Marc S.-
dc.contributor.authorTanaka, Nobuyuki-
dc.contributor.authorOishi, Isao-
dc.contributor.authorAizawa, Shinichi-
dc.contributor.authorMatsuyama, Toshifumi-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorTaki, Shinsuke-
dc.contributor.authorTaniguchi, Tadatsugu-
dc.date.accessioned2020-11-17T14:54:17Z-
dc.date.available2020-11-17T14:54:17Z-
dc.date.issued1997-
dc.identifier.citationLeukemia, 1997, v. 11, n. SUPPL. 3, p. 439-440-
dc.identifier.issn0887-6924-
dc.identifier.urihttp://hdl.handle.net/10722/291398-
dc.description.abstractLymphocytes are highly sensitive to DNA damage-induced apoptosis. In thymocytes, the tumor suppressor p53 has been shown to be required for this type of apoptosis. However an as yet unknown, p53-independent pathway(s) appears to mediate the same event in mitogenically activated mature T lymphocytes. By using mice with a null mutation in the IRF-1 gene, we revealed that DNA damage-induced apoptosis in the latter cell type is dependent on the anti-oncogenic transcription factor interferon regulatory factor-1 (IRF-1). Thus two different anti-oncogenic transcription factors, p53 and IRF-1, are required for distinct apoptotic pathways in T lymphocytes. Furthermore, we found that mitogen induction of the interleukin-1β-converting enzyme (Ice) gene, a mammalian homolog of the Caenorhabditis elegans cell death gene ced-3, is also IRF-1-dependent. An IRF-1 binding sequence was identified in the 5′ flanking region of the Ice gene. In addition, ectopic overexpression of IRF-1 results in the activation of the endogenous Ice gene and enhances the sensitivity of cells to radiation-induced apoptosis. Thus, induction of Ice gene may be involved in IRF-1 dependent DNA damage-induced apoptosis in activated mature T lymphocytes.-
dc.languageeng-
dc.relation.ispartofLeukemia-
dc.titleDNA damage-induced apoptosis and ice gene induction in mitogenically activated T lymphocytes require IRF-1-
dc.typeArticle-
dc.identifier.pmid9209417-
dc.identifier.scopuseid_2-s2.0-0030769379-
dc.identifier.volume11-
dc.identifier.issueSUPPL. 3-
dc.identifier.spage439-
dc.identifier.epage440-
dc.identifier.issnl0887-6924-

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