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  1. 010 学術雑誌論文
  2. 田辺, 秀之 / TANABE, Hideyuki

Requirement of wild-type p53 protein for maintenance of chromosomal integrity

https://ir.soken.ac.jp/records/3984
https://ir.soken.ac.jp/records/3984
a8cfda9e-b381-404e-b7cc-d4e9274ee68f
Item type 学術雑誌論文 / Journal Article(1)
公開日 2013-09-25
タイトル
タイトル Requirement of wild-type p53 protein for maintenance of chromosomal integrity
タイトル
言語 en
タイトル Requirement of wild-type p53 protein for maintenance of chromosomal integrity
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 HONMA, Masamitsu

× HONMA, Masamitsu

WEKO 2109

HONMA, Masamitsu

Search repository
MOMOSE, Maki

× MOMOSE, Maki

WEKO 2129

MOMOSE, Maki

Search repository
TANABE, Hideyuki

× TANABE, Hideyuki

WEKO 368

TANABE, Hideyuki

Search repository
SAKAMOTO, Hiroko

× SAKAMOTO, Hiroko

WEKO 2111

SAKAMOTO, Hiroko

Search repository
YU, Yongjia

× YU, Yongjia

WEKO 2130

YU, Yongjia

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LITTLE, John B

× LITTLE, John B

WEKO 2131

LITTLE, John B

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SOFUNI, Toshio

× SOFUNI, Toshio

WEKO 2132

SOFUNI, Toshio

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HAYASHI, Makoto

× HAYASHI, Makoto

WEKO 2108

HAYASHI, Makoto

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著者別名 田辺, 秀之

× 田辺, 秀之

WEKO 367
NRID 1000050261178
e-Rad 50261178

田辺, 秀之

Search repository
抄録
内容記述タイプ Abstract
内容記述 Chromosomal double-strand breaks (DSBs) occurring in mammalian cells can initiate genomic instability, and their misrepairs result in chromosomal deletion, amplification, and translocation, common findings in human tumors. The tumor-suppressor protein p53 is involved in maintaining genomic stability. In this study, we demonstrate that the deficiency of wild-type p53 protein may allow unrepaired DSBs to initiate chromosomal instability. The human lymphoblastoid cell line TK6-E6 was established by transfection with human papilloma virus 16 (HPV16) E6 cDNA into parental TK6 cells via a retroviral vector. Abrogation of p53 function by E6 resulted in an increase in the spontaneous mutation frequencies at the heterozygous thymidine kinase (TK) locus but not at the hemizygous hypoxanthine phosphoribosyl transferase (HPRT) locus. Almost all TK-deficient mutants from TK6-E6 cells exhibited loss of heterozygosity (LOH) with the hemizygous TK allele. LOH analysis with microsatellite loci spanning the long arm of chromosome 17, which harbors the TK locus, showed that LOH extended over half of 17q toward the terminal end. Cytogenetic analysis of LOH mutants by chromosome painting indicated a mosaic of chromosomal aberrations involving chromosome 17, in which partial chromosome deletions, amplifications, and multiple translocations appeared heterogeneously in a single mutant. We speculate that spontaneous DSBs trigger the breakage-fusion bridge cycle leading to such multiple chromosome aberrations. In contrast, no chromosomal alterations were observed in TK-deficient mutants from TK6-20C cells expressing wild-type p53. In wild-type p53 cells, spontaneous DSBs appear to be promptly repaired through recombination between homologous chromosomes. These results support a model in which p53 protein contributes to the maintenance of genomic integrity through recombinational repair.
書誌情報 Molecular Carcinogenesis
en : Molecular Carcinogenesis

巻 28, 号 4, p. 203-214, 発行日 2000-08
出版者
出版者 Wiley-Blackwell
ISSN
収録物識別子タイプ ISSN
収録物識別子 0899-1987
DOI
識別子タイプ DOI
関連識別子 https://doi.org/10.1002/1098-2744(200008)28:4<203::AID-MC3>3.0.CO;2-1
関連名称 10.1002/1098-2744(200008)28:4<203::AID-MC3>3.0.CO;2-1
権利
権利情報 © 2000 Wiley-Liss, Inc
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