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KAISO, a critical regulator of p53-mediated transcription of CDKN1A and apoptotic genes

Authors
 Dong-In Koh  ;  Dohyun Han  ;  Hoon Ryu  ;  Won-Il Choi  ;  Bu-Nam Jeon  ;  Min-Kyeong Kim  ;  Youngsoo Kim  ;  Jin Young Kim  ;  Lee Parry  ;  Alan R. Clarke  ;  Albert B. Reynolds  ;  Man-Wook Hur 
Citation
 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol.111(42) : 15078-15083, 2014 
Journal Title
 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 
ISSN
 0027-8424 
Issue Date
2014
MeSH
Acetylation ; Animals ; Apoptosis* ; Cell Cycle ; Cell Line ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p21/metabolism* ; DNA/chemistry ; DNA Damage ; DNA Methylation ; E1A-Associated p300 Protein/metabolism ; Female ; Fibroblasts/cytology ; HCT116 Cells ; HEK293 Cells ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Promoter Regions, Genetic ; Protein Binding ; Response Elements ; Transcription Factors/metabolism* ; Tumor Suppressor Protein p53/metabolism*
Keywords
KAISO ; apoptosis ; cell cycle arrest ; p300 ; p53
Abstract
An unresolved issue in genotoxic stress response is identification of induced regulatory proteins and how these activate tumor suppressor p53 to determine appropriate cell responses. Transcription factor KAISO was previously described to repress transcription following binding to methylated DNA. In this study, we show that KAISO is induced by DNA damage in p53-expressing cells and then interacts with the p53–p300 complex to increase acetylation of p53 K320 and K382 residues, although decreasing K381 acetylation. Moreover, the p53 with this particular acetylation pattern shows increased DNA binding and potently induces cell cycle arrest and apoptosis by activating transcription of CDKN1A (cyclin-dependent kinase inhibitor 1) and various apoptotic genes. Analogously, in Kaiso KO mouse embryonic fibroblast cells, p53-to-promoter binding and up-regulation of p21 and apoptosis gene expression is significantly compromised. KAISO may therefore be a critical regulator of p53-mediated cell cycle arrest and apoptosis in response to various genotoxic stresses in mammalian cells.
Full Text
http://www.pnas.org/content/111/42/15078.long
DOI
10.1073/pnas.1318780111
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Min Kyeong(김민경)
Jeon, Bu Nam(전부남)
Choi, Won Il(최원일)
Hur, Man Wook(허만욱) ORCID logo https://orcid.org/0000-0002-3416-1334
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/100129
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