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Phenylbutyric acid induces the cellular senescence through an Akt/p21(WAF1) signaling pathway

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dc.contributor.authorKim, Hag Dong-
dc.contributor.authorJang, Chang-Young-
dc.contributor.authorChoe, Jeong Min-
dc.contributor.authorSohn, Jeongwon-
dc.contributor.authorKim, Joon-
dc.date.accessioned2021-09-06T18:54:17Z-
dc.date.available2021-09-06T18:54:17Z-
dc.date.created2021-06-18-
dc.date.issued2012-06-01-
dc.identifier.issn0006-291X-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/108176-
dc.description.abstractIt has been well known that three sentinel proteins - PERK, ATF6 and IRE1 - initiate the unfolded protein response (UPR) in the presence of misfolded or unfolded proteins in the ER. Recent studies have demonstrated that upregulation of UPR in cancer cells is required to survive and proliferate. Here, we showed that long exposure to 4-phenylbutyric acid (PBA), a chemical chaperone that can reduce retention of unfolded and misfolded proteins in ER, induced cellular senescence in cancer cells such as MCF7 and HT1080. In addition, we found that treatment with PBA activates Akt, which results in p21(WAF1) induction. Interestingly, the depletion of PERK but not ATF6 and IRE1 also induces cellular senescence, which was rescued by additional depletion of Akt. This suggests that Akt pathway is downstream of PERK in PBA induced cellular senescence. Taken together, these results show that PBA induces cellular senescence via activation of the Akt/p21(WAF1) pathway by PERK inhibition. (C) 2012 Elsevier Inc. All rights reserved.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE-
dc.subjectENDOPLASMIC-RETICULUM STRESS-
dc.subjectUNFOLDED-PROTEIN RESPONSE-
dc.subjectER STRESS-
dc.subjectTRANSMEMBRANE PROTEIN-
dc.subjectTRANSCRIPTION FACTOR-
dc.subjectOXIDATIVE STRESS-
dc.subjectAPOPTOSIS-
dc.subjectGENES-
dc.subjectATF6-
dc.subjectIDENTIFICATION-
dc.titlePhenylbutyric acid induces the cellular senescence through an Akt/p21(WAF1) signaling pathway-
dc.typeArticle-
dc.contributor.affiliatedAuthorSohn, Jeongwon-
dc.contributor.affiliatedAuthorKim, Joon-
dc.identifier.doi10.1016/j.bbrc.2012.04.086-
dc.identifier.scopusid2-s2.0-84861668798-
dc.identifier.wosid000305300800002-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.422, no.2, pp.213 - 218-
dc.relation.isPartOfBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.citation.titleBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.citation.volume422-
dc.citation.number2-
dc.citation.startPage213-
dc.citation.endPage218-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaBiophysics-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiophysics-
dc.subject.keywordPlusENDOPLASMIC-RETICULUM STRESS-
dc.subject.keywordPlusUNFOLDED-PROTEIN RESPONSE-
dc.subject.keywordPlusER STRESS-
dc.subject.keywordPlusTRANSMEMBRANE PROTEIN-
dc.subject.keywordPlusTRANSCRIPTION FACTOR-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusAPOPTOSIS-
dc.subject.keywordPlusGENES-
dc.subject.keywordPlusATF6-
dc.subject.keywordPlusIDENTIFICATION-
dc.subject.keywordAuthorCellular senescence-
dc.subject.keywordAuthorER stress-
dc.subject.keywordAuthorPBA-
dc.subject.keywordAuthorAkt-
dc.subject.keywordAuthorPERK-
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