p53-mediated apoptosis is attenuated in Werner syndrome cells

被引：138

作者：

Spillare, EA

Robles, AI

Wang, XW

Shen, JC

Yu, CE

Schellenberg, GD

Harris, CC

机构：

[1] NCI, Human Carcinogenesis Lab, Bethesda, MD 20892 USA

[2] Univ Washington, Dept Pathol, Seattle, WA 98195 USA

[3] Vet Affairs Puget Sound Hlth Care Syst, Geriatr Res Educ & Clin Ctr 182B, Seattle Div, Seattle, WA 98108 USA

来源：

GENES & DEVELOPMENT | 1999年 / 13卷 / 11期

关键词：

DNA helicase; XPB; XPD; p53 carboxy-terminal domain;

D O I：

10.1101/gad.13.11.1355

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The WRN DNA helicase is a member of the DExH-containing DNA helicase superfamily that includes XPB, XPD, and BLM. Mutations in WRN are found in patients with the premature aging and cancer susceptibility syndrome known as Werner syndrome (WS). p53 binds to the WRN protein in vivo and in vitro through its carboxyl terminus. WS fibroblasts have an attenuated p53-mediated apoptotic response, and this deficiency can be rescued by expression of wild-type WRN. These data support the hypothesis that p53 can induce apoptosis through the modulation of specific DExH-containing DNA helicases and may have implications for the cancer predisposition observed in WS patients.

引用

收藏

页码：1355 / 1360

页数：6

相关论文

共 29 条

[1] THYMOCYTE APOPTOSIS INDUCED BY P53-DEPENDENT AND INDEPENDENT PATHWAYS [J].

CLARKE, AR ;

PURDIE, CA ;

HARRISON, DJ ;

MORRIS, RG ;

BIRD, CC ;

HOOPER, ML ;

WYLLIE, AH .

NATURE, 1993, 362 (6423) :849-852

[2] A BIOMARKER THAT IDENTIFIES SENESCENT HUMAN-CELLS IN CULTURE AND IN AGING SKIN IN-VIVO [J].

DIMRI, GP ;

LEE, XH ;

BASILE, G ;

ACOSTA, M ;

SCOTT, C ;

ROSKELLEY, C ;

MEDRANO, EE ;

LINSKENS, M ;

RUBELJ, I ;

PEREIRASMITH, O ;

PEACOCKE, M ;

CAMPISI, J .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (20) :9363-9367

[3] DNA helicases in inherited human disorders [J].

Ellis, NA .

CURRENT OPINION IN GENETICS & DEVELOPMENT, 1997, 7 (03) :354-363

[4] Hepatitis B virus X protein and p53 tumor suppressor interactions in the modulation of apoptosis [J].

Elmore, LW ;

Hancock, AR ;

Chang, SF ;

Wang, XW ;

Chang, S ;

Callahan, CP ;

Geller, DA ;

Will, H ;

Harris, CC .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (26) :14707-14712

[5] WERNERS SYNDROME - A REVIEW OF ITS SYMPTOMATOLOGY NATURAL HISTORY PATHOLOGIC FEATURES GENETICS AND RELATIONSHIP TO NATURAL AGING PROCESS [J].

EPSTEIN, CJ ;

MARTIN, GM ;

SCHULTZ, AL ;

MOTULSKY, AG .

MEDICINE, 1966, 45 (03) :177-+

[6] Analysis of helicase gene mutations in Japanese Werner's syndrome patients [J].

Goto, M ;

Imamura, O ;

Kuromitsu, J ;

Matsumoto, T ;

Yamabe, Y ;

Tokutake, Y ;

Suzuki, N ;

Mason, B ;

Drayna, D ;

Sugawara, M ;

Sugimoto, M ;

Furuichi, Y .

HUMAN GENETICS, 1997, 99 (02) :191-193

[7]

Goto M, 1996, CANCER EPIDEM BIOMAR, V5, P239

[8] The Werner syndrome protein is a DNA helicase [J].

Gray, MD ;

Shen, JC ;

KamathLoeb, AS ;

Blank, A ;

Sopher, BL ;

Martin, GM ;

Oshima, J ;

Loeb, LA .

NATURE GENETICS, 1997, 17 (01) :100-103

[9] P53 MUTATIONS IN HUMAN CANCERS [J].

HOLLSTEIN, M ;

SIDRANSKY, D ;

VOGELSTEIN, B ;

HARRIS, CC .

SCIENCE, 1991, 253 (5015) :49-53

[10] The premature ageing syndrome protein, WRN, is a 3′→5′ exonuclease [J].

Huang, SR ;

Li, BM ;

Gray, MD ;

Oshima, J ;

Mian, SI ;

Campisi, J .

NATURE GENETICS, 1998, 20 (02) :114-116