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Article: Cellular commitment to oncogene-induced transformation or apoptosis is dependent on the transcription factor IRF-1

TitleCellular commitment to oncogene-induced transformation or apoptosis is dependent on the transcription factor IRF-1
Authors
Issue Date1994
Citation
Cell, 1994, v. 77, n. 6, p. 829-839 How to Cite?
AbstractThe transcriptional activator interferon regulatory factor 1 (IRF-1) and its antagonistic repressor IRF-2 are regulators of the interferon (IFN) system and of cell growth. Here we report that embryonic fibroblasts (EFs) from mice with a null mutation in the IRF-1 gene (IRF-1-/- mice) can be transformed by expression of an activated c-Ha-ras oncogene. This property is not observed in EFs from wild-type or IRF-2-/- mice but is still observed in EFs from mice deficient in both genes. The transformed phenotype of ras-expressing IRF-1-/- EFs could be suppressed by the expression of the IRF-1 cDNA. Thus, IRF-1 functions as a tumor suppressor. Furthermore, expression of the c-Ha-ras oncogene causes wild-type but not IRF-1-/- EFs to undergo apoptosis when combined with a block to cell proliferation or treated by anticancer drugs or ionizing radiation. Hence, IRF-1 may be a critical determinant of oncogene-induced cell transformation or apoptosis. © 1994.
Persistent Identifierhttp://hdl.handle.net/10722/292444
ISSN
2023 Impact Factor: 45.5
2023 SCImago Journal Rankings: 24.342
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTanaka, Nobuyuki-
dc.contributor.authorIshihara, Masahiko-
dc.contributor.authorKitagawa, Motoo-
dc.contributor.authorHarada, Hisashi-
dc.contributor.authorKimura, Tohru-
dc.contributor.authorMatsuyama, Toshifumi-
dc.contributor.authorLamphier, Marc S.-
dc.contributor.authorAizawa, Shinichi-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorTaniguchi, Tadatsugu-
dc.date.accessioned2020-11-17T14:56:30Z-
dc.date.available2020-11-17T14:56:30Z-
dc.date.issued1994-
dc.identifier.citationCell, 1994, v. 77, n. 6, p. 829-839-
dc.identifier.issn0092-8674-
dc.identifier.urihttp://hdl.handle.net/10722/292444-
dc.description.abstractThe transcriptional activator interferon regulatory factor 1 (IRF-1) and its antagonistic repressor IRF-2 are regulators of the interferon (IFN) system and of cell growth. Here we report that embryonic fibroblasts (EFs) from mice with a null mutation in the IRF-1 gene (IRF-1-/- mice) can be transformed by expression of an activated c-Ha-ras oncogene. This property is not observed in EFs from wild-type or IRF-2-/- mice but is still observed in EFs from mice deficient in both genes. The transformed phenotype of ras-expressing IRF-1-/- EFs could be suppressed by the expression of the IRF-1 cDNA. Thus, IRF-1 functions as a tumor suppressor. Furthermore, expression of the c-Ha-ras oncogene causes wild-type but not IRF-1-/- EFs to undergo apoptosis when combined with a block to cell proliferation or treated by anticancer drugs or ionizing radiation. Hence, IRF-1 may be a critical determinant of oncogene-induced cell transformation or apoptosis. © 1994.-
dc.languageeng-
dc.relation.ispartofCell-
dc.titleCellular commitment to oncogene-induced transformation or apoptosis is dependent on the transcription factor IRF-1-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/0092-8674(94)90132-5-
dc.identifier.pmid8004672-
dc.identifier.scopuseid_2-s2.0-0028276685-
dc.identifier.volume77-
dc.identifier.issue6-
dc.identifier.spage829-
dc.identifier.epage839-
dc.identifier.isiWOS:A1994NT33100008-
dc.identifier.issnl0092-8674-

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