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Article: p53-dependent inhibition of FKHRL1 in response to DNA damage through protein kinase SGK1

Titlep53-dependent inhibition of FKHRL1 in response to DNA damage through protein kinase SGK1
Authors
Issue Date2004
Citation
Proceedings of the National Academy of Sciences of the United States of America, 2004, v. 101, n. 39, p. 14057-14062 How to Cite?
AbstractFKHRL1 (FOXO3a) and p53 are two potent stress-response regulators. Here we show that these two transcription factors exhibit "crosstalk" in vivo. In response to DNA damage, p53 activation led to FKHRL1 phosphorylation and subcellular localization change, which resulted in inhibition of FKHRL1 transcription activity. AKT was dispensable for p53-dependent suppression of FKHRL1. By contrast, serum- and glucocorticoid-inducible kinase 1 (SGK1) was significantly induced in a p53-dependent manner after DNA damage, and this induction was through extracellular signal-regulated kinase 1/2-mediated posttranslational regulation. Furthermore, inhibition of SGK1 expression by a small interfering RNA knockdown experiment significantly decreased FKHRL1 phosphorylation in response to DNA damage. Taken together, our observations reveal previously unrecognized crosstalk between p53 and FKHRL1. Moreover, our findings suggest a new pathway for understanding aging and the age dependency of human diseases governed by these two transcription factors.
Persistent Identifierhttp://hdl.handle.net/10722/291837
ISSN
2020 Impact Factor: 11.205
2020 SCImago Journal Rankings: 5.011
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYou, Han-
dc.contributor.authorJang, Ying Ju-
dc.contributor.authorYou-Ten, Annick Itie-
dc.contributor.authorOkada, Hitoshi-
dc.contributor.authorLiepa, Jennifer-
dc.contributor.authorWakeham, Andrew-
dc.contributor.authorZaugg, Kathrin-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:55:13Z-
dc.date.available2020-11-17T14:55:13Z-
dc.date.issued2004-
dc.identifier.citationProceedings of the National Academy of Sciences of the United States of America, 2004, v. 101, n. 39, p. 14057-14062-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10722/291837-
dc.description.abstractFKHRL1 (FOXO3a) and p53 are two potent stress-response regulators. Here we show that these two transcription factors exhibit "crosstalk" in vivo. In response to DNA damage, p53 activation led to FKHRL1 phosphorylation and subcellular localization change, which resulted in inhibition of FKHRL1 transcription activity. AKT was dispensable for p53-dependent suppression of FKHRL1. By contrast, serum- and glucocorticoid-inducible kinase 1 (SGK1) was significantly induced in a p53-dependent manner after DNA damage, and this induction was through extracellular signal-regulated kinase 1/2-mediated posttranslational regulation. Furthermore, inhibition of SGK1 expression by a small interfering RNA knockdown experiment significantly decreased FKHRL1 phosphorylation in response to DNA damage. Taken together, our observations reveal previously unrecognized crosstalk between p53 and FKHRL1. Moreover, our findings suggest a new pathway for understanding aging and the age dependency of human diseases governed by these two transcription factors.-
dc.languageeng-
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of America-
dc.titlep53-dependent inhibition of FKHRL1 in response to DNA damage through protein kinase SGK1-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1073/pnas.0406286101-
dc.identifier.pmid15383658-
dc.identifier.pmcidPMC521120-
dc.identifier.scopuseid_2-s2.0-4644279286-
dc.identifier.volume101-
dc.identifier.issue39-
dc.identifier.spage14057-
dc.identifier.epage14062-
dc.identifier.isiWOS:000224211400019-
dc.identifier.issnl0027-8424-

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