File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: An IRF-1-dependent pathway of DNA damage-induced apoptosis in mitogen-activated T lymphocytes

TitleAn IRF-1-dependent pathway of DNA damage-induced apoptosis in mitogen-activated T lymphocytes
Authors
Issue Date1995
Citation
Nature, 1995, v. 376, n. 6541, p. 596-599 How to Cite?
AbstractLymphocytes are particularly susceptible to DNA damage-induced apoptosis, a response which may serve as a form of ‘altruistic suicide ’ to counter their intrinsic high potential for mutation and clonal expansion1. The tumour suppressor p53 has been shown to regulate this type of apoptosis in thymocytes2,3, but an as yet unknown, p53-independent pathway(s) appears to mediate the same event in mitogen-activated mature T lymphocytes4. Here we show that DNA damage-induced apoptosis in these T lymphocytes is dependent on the antioncogenic transcription factor interferon regulatory factor (IRF)-l (refs 5-7). Thus two different anti-onco-genic transcription factors, p53 and IRF-1, are required for distinct apoptotic pathways in T lymphocytes. We also show that mitogen induction of the interleukin-lβ converting enzyme (ICE) gene8á-10, a mammalian homologue of the Caenorhabditis elegans cell death gene ced-3, is IRF-1-dependent. Ectopic overexpression of IRF-1 results in the activation of the endogenous gene for ICE and enhances the sensitivity of cells to radiation-induced apoptosis. © 1995, Nature Publishing Group. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/292478
ISSN
2023 Impact Factor: 50.5
2023 SCImago Journal Rankings: 18.509
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTamura, Tomohiko-
dc.contributor.authorIshihara, Masahiko-
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.accessioned2020-11-17T14:56:34Z-
dc.date.available2020-11-17T14:56:34Z-
dc.date.issued1995-
dc.identifier.citationNature, 1995, v. 376, n. 6541, p. 596-599-
dc.identifier.issn0028-0836-
dc.identifier.urihttp://hdl.handle.net/10722/292478-
dc.description.abstractLymphocytes are particularly susceptible to DNA damage-induced apoptosis, a response which may serve as a form of ‘altruistic suicide ’ to counter their intrinsic high potential for mutation and clonal expansion1. The tumour suppressor p53 has been shown to regulate this type of apoptosis in thymocytes2,3, but an as yet unknown, p53-independent pathway(s) appears to mediate the same event in mitogen-activated mature T lymphocytes4. Here we show that DNA damage-induced apoptosis in these T lymphocytes is dependent on the antioncogenic transcription factor interferon regulatory factor (IRF)-l (refs 5-7). Thus two different anti-onco-genic transcription factors, p53 and IRF-1, are required for distinct apoptotic pathways in T lymphocytes. We also show that mitogen induction of the interleukin-lβ converting enzyme (ICE) gene8á-10, a mammalian homologue of the Caenorhabditis elegans cell death gene ced-3, is IRF-1-dependent. Ectopic overexpression of IRF-1 results in the activation of the endogenous gene for ICE and enhances the sensitivity of cells to radiation-induced apoptosis. © 1995, Nature Publishing Group. All Rights Reserved.-
dc.languageeng-
dc.relation.ispartofNature-
dc.titleAn IRF-1-dependent pathway of DNA damage-induced apoptosis in mitogen-activated T lymphocytes-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/376596a0-
dc.identifier.pmid7637809-
dc.identifier.scopuseid_2-s2.0-0029144891-
dc.identifier.volume376-
dc.identifier.issue6541-
dc.identifier.spage596-
dc.identifier.epage599-
dc.identifier.isiWOS:A1995RP75600052-
dc.identifier.issnl0028-0836-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats