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Titolo:
UV-induced skin carcinogenesis in xeroderma pigmentosum group A (XPA) gene-knockout mice with nucleotide excision repair-deficiency
Autore:
Tanaka, K; Kamiuchi, S; Ren, Y; Yonemasu, R; Ichikawa, M; Murai, H; Yoshino, M; Takeuchi, S; Saijo, M; Nakatsu, Y; Miyauchi-Hashimoto, H; Horio, T;
Indirizzi:
Osaka Univ, Inst Mol & Cellular Biol, Suita, Osaka 5650871, Japan Osaka Univ Suita Osaka Japan 5650871 ar Biol, Suita, Osaka 5650871, Japan Japan Sci & Technol Corp, CREST, Suita, Osaka 5650871, Japan Japan Sci & Technol Corp Suita Osaka Japan 5650871 , Osaka 5650871, Japan Kansai Med Univ, Dept Dermatol, Osaka 5708507, Japan Kansai Med Univ Osaka Japan 5708507 Dept Dermatol, Osaka 5708507, Japan
Titolo Testata:
MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
fascicolo: 1-2, volume: 477, anno: 2001,
pagine: 31 - 40
SICI:
1386-1964(20010602)477:1-2<31:USCIXP>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
RNA-POLYMERASE-II; COUPLING FACTOR CSB/ERCC6; A COMPLEMENTING PROTEIN; RPA-BINDING DOMAIN; IN-VIVO MUTATIONS; DNA-REPAIR; COCKAYNE-SYNDROME; ULTRAVIOLET-B; ELONGATION COMPLEXES; DAMAGE-RECOGNITION;
Keywords:
Xeroderma pigmentosum; nucleotide excision repair; knockout mice; UV-induced skin carcinogenesis and mutagenesis; UV-induced immunosuppression;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
63
Recensione:
Indirizzi per estratti:
Indirizzo: Tanaka, K Osaka Univ, Inst Mol & Cellular Biol, 1-3 Yamadaoka, Suita, Osaka 5650871,Japan Osaka Univ 1-3 Yamadaoka Suita Osaka Japan 5650871 5650871,Japan
Citazione:
K. Tanaka et al., "UV-induced skin carcinogenesis in xeroderma pigmentosum group A (XPA) gene-knockout mice with nucleotide excision repair-deficiency", MUT RES-F M, 477(1-2), 2001, pp. 31-40

Abstract

Nucleotide excision repair (NER) removes a wide variety of lesions from the genome and is deficient in the genetic disorder, xeroderma pigmentosum (XP). In this paper, an in vitro analysis of the XP group A gene product (XPAprotein) is reported. Results of an analysis on the pathogenesis of ultraviolet (UV)-B-induced skin cancer in the XPA gene-knockout mouse are also described: (1) contrary to wild type mice, significant bias of p53 mutations to the transcribed strand and no evident p53 mutational hot spots were detected in the skin tumors of XPA-knockout mice. (2) Skin cancer cell lines from UVB-irradiated XPA-knockout mice had a decreased mismatch repair activity and an abnormal cell cycle checkpoint, suggesting that the downregulationof mismatch repair helps cells escape killing by UVB and that mismatch repair-deficient clones are selected for during the tumorigenic transformationof XPA (-/-) cells. (3) The XPA-knockout mice showed a higher frequency ofUVB-induced mutation in the rpsL transgene at a low dose of UVB-irradiation than the wild type mice. CC --> TT tandem transition, a hallmark of UV-induced mutation, was detected at higher frequency in the rpsL transgene in the XPA-knockout mice than the wild type mice. This rpsL/XPA mouse system will be useful for further analysing the role of NER in the mutagenesis induced by various carcinogens. (4) The UVB-induced immunosuppression was greatly enhanced in the XPA-knockout mice. It is possible that an enhanced impairment of the immune system by UVB irradiation is involved in the high incidence of skin cancer in XP. (C) 2001 Elsevier Science B.V. All rights reserved.

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Documento generato il 07/07/20 alle ore 15:45:32