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- Publisher Website: 10.1038/382816a0
- Scopus: eid_2-s2.0-16044362508
- PMID: 8752276
- WOS: WOS:A1996VE34700049
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Article: Cooperation of the tumour suppressors IRF-1 and p53 in response to DNA damage
Title | Cooperation of the tumour suppressors IRF-1 and p53 in response to DNA damage |
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Authors | |
Issue Date | 1996 |
Citation | Nature, 1996, v. 382, n. 6594, p. 816-818 How to Cite? |
Abstract | NORMALLY growing cells promptly cease DNA synthesis when exposed to genotoxic stresses, such as radiation, and this cell-cycle arrest prevents the accumulation of mutations. The transcription factor interferon regulatory factor (IRF)-1 is essential for the regulation of the interferon system, inhibits cell growth, and manifests tumour-suppressor activities. Here we show that mouse embryonic fibroblasts (EFs) lacking IRF-1 are deficient in their ability to undergo DNA-damage-induced cell-cycle arrest. A similar phenotype has been observed in EFs lacking the turnout suppressor p53 (refs 8, 9), although the expression of IRF-1 and p53 are independent of one another. Furthermore, we show that transcriptional induction of the gene encoding p21 (WAF1, CIP1), a cell-cycle inhibitor, by γ-irradiation is dependent on both p53 and IRF-1, and that the p21 promoter is activated, either directly or indirectly, by both in a transient cotransfection assay. These two tumour-suppressor transcription factors therefore converge functionally to regulate the cell cycle through the activation of a common target genes. |
Persistent Identifier | http://hdl.handle.net/10722/291703 |
ISSN | 2023 Impact Factor: 50.5 2023 SCImago Journal Rankings: 18.509 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Tanaka, N. | - |
dc.contributor.author | Ishihara, M. | - |
dc.contributor.author | Lamphier, M. S. | - |
dc.contributor.author | Nozawa, H. | - |
dc.contributor.author | Matsuyama, T. | - |
dc.contributor.author | Mak, T. W. | - |
dc.contributor.author | Aizawa, S. | - |
dc.contributor.author | Tokino, T. | - |
dc.contributor.author | Oren, M. | - |
dc.contributor.author | Taniguchi, T. | - |
dc.date.accessioned | 2020-11-17T14:54:56Z | - |
dc.date.available | 2020-11-17T14:54:56Z | - |
dc.date.issued | 1996 | - |
dc.identifier.citation | Nature, 1996, v. 382, n. 6594, p. 816-818 | - |
dc.identifier.issn | 0028-0836 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291703 | - |
dc.description.abstract | NORMALLY growing cells promptly cease DNA synthesis when exposed to genotoxic stresses, such as radiation, and this cell-cycle arrest prevents the accumulation of mutations. The transcription factor interferon regulatory factor (IRF)-1 is essential for the regulation of the interferon system, inhibits cell growth, and manifests tumour-suppressor activities. Here we show that mouse embryonic fibroblasts (EFs) lacking IRF-1 are deficient in their ability to undergo DNA-damage-induced cell-cycle arrest. A similar phenotype has been observed in EFs lacking the turnout suppressor p53 (refs 8, 9), although the expression of IRF-1 and p53 are independent of one another. Furthermore, we show that transcriptional induction of the gene encoding p21 (WAF1, CIP1), a cell-cycle inhibitor, by γ-irradiation is dependent on both p53 and IRF-1, and that the p21 promoter is activated, either directly or indirectly, by both in a transient cotransfection assay. These two tumour-suppressor transcription factors therefore converge functionally to regulate the cell cycle through the activation of a common target genes. | - |
dc.language | eng | - |
dc.relation.ispartof | Nature | - |
dc.title | Cooperation of the tumour suppressors IRF-1 and p53 in response to DNA damage | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1038/382816a0 | - |
dc.identifier.pmid | 8752276 | - |
dc.identifier.scopus | eid_2-s2.0-16044362508 | - |
dc.identifier.volume | 382 | - |
dc.identifier.issue | 6594 | - |
dc.identifier.spage | 816 | - |
dc.identifier.epage | 818 | - |
dc.identifier.isi | WOS:A1996VE34700049 | - |
dc.identifier.issnl | 0028-0836 | - |