Cited 8 times in
KLHL4, a novel p53 target gene, inhibits cell proliferation by activating p21 WAF/CDKN1A
DC Field | Value | Language |
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dc.contributor.author | 허만욱 | - |
dc.date.accessioned | 2020-12-01T17:21:35Z | - |
dc.date.available | 2020-12-01T17:21:35Z | - |
dc.date.issued | 2020-09 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/180231 | - |
dc.description.abstract | KLHL4 is a member of the KLHL protein family, many of whom bind the Cul3 E3 ligase, and mediate the ubiquitination of interacting proteins. The KLHL4 gene, localized on the X chromosome, associates with a disorder known as X-linked cleft palate (CPX). However, the biological functions of KLHL4 are largely unknown. In this study, microarray analysis of HEK293A embryonic kidney cells, expressing ectopic p53, showed a 3-fold increase of KLHL4 mRNA. Moreover, both KLHL4 mRNA and protein expression were elevated by p53 or DNA damage, suggesting that KLHL4 might be a p53 target gene. We also found that KLHL4 activates transcription of p21WAF/CDKN1A, a p53 target gene encoding a major negative regulator of the cell-cycle. KLHL4 interacted with p53 to increase its binding to p53 response element of the p21WAF/CDKN1A gene, resulting in transcriptional upregulation. Furthermore, we observed that KLHL4 can interact with the Cul3 ubiquitin ligase, to possibly play a role in ubiquitin-mediated proteasomal degradation, and Klhl4 knocked-out MEF mouse embryonic fibroblasts proliferated faster than WT MEF cells. These results suggest that KLHL4 upregulation by p53 may inhibit cell proliferation, by activating p21WAF/CDKN1A. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.language | English | - |
dc.publisher | Elsevier | - |
dc.relation.isPartOf | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.title | KLHL4, a novel p53 target gene, inhibits cell proliferation by activating p21 WAF/CDKN1A | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) | - |
dc.contributor.googleauthor | Seo-Hyun Choi | - |
dc.contributor.googleauthor | Su-Yeon Cho | - |
dc.contributor.googleauthor | Jiyang Song | - |
dc.contributor.googleauthor | Man-Wook Hur | - |
dc.identifier.doi | 10.1016/j.bbrc.2020.07.100 | - |
dc.contributor.localId | A04350 | - |
dc.relation.journalcode | J00281 | - |
dc.identifier.eissn | 1090-2104 | - |
dc.identifier.pmid | 32753315 | - |
dc.identifier.url | https://www.sciencedirect.com/science/article/pii/S0006291X20314972 | - |
dc.subject.keyword | Cell proliferation | - |
dc.subject.keyword | Cullin | - |
dc.subject.keyword | DNA damage | - |
dc.subject.keyword | KLHL4 | - |
dc.subject.keyword | Ubiquitination | - |
dc.subject.keyword | p21 | - |
dc.subject.keyword | p53 | - |
dc.contributor.alternativeName | Hur, Man Wook | - |
dc.contributor.affiliatedAuthor | 허만욱 | - |
dc.citation.volume | 530 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 588 | - |
dc.citation.endPage | 596 | - |
dc.identifier.bibliographicCitation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.530(3) : 588-596, 2020-09 | - |
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