Tumour suppressor p53: understanding the molecular mechanisms inherent to cancer

被引：0

作者：

Kumari, Rajni ^{[1
]}

Sen, Nirmalya ^{[1
]}

Das, Sanjeev ^{[1
]}

机构：

[1] Natl Inst Immunol, Mol Oncol Lab, New Delhi 110067, India

来源：

CURRENT SCIENCE | 2014年 / 107卷 / 05期

关键词：

Cancer; molecular mechanisms; stress signals; tumour suppressor genes; CELL-CYCLE ARREST; DNA-DAMAGE; GENE-EXPRESSION; IN-VITRO; P53-DEPENDENT APOPTOSIS; P53-INDUCIBLE REGULATOR; TRANSCRIPTION FACTOR; POTENTIAL MEDIATOR; REACTIVE OXYGEN; KINASE-ACTIVITY;

D O I：

暂无

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Tumour suppressor p53 has been the centre of focus of researchers trying to decipher the molecular mechanisms underlying tumourigenesis. In this review, we have summarized the critical role of p53 in tumour suppression through its effects on several cellular processes such as DNA repair, cell cycle and apoptosis. We have also discussed the role of upstream regulators which sensitize p53 to respond to different stress conditions. Post-translational modifications of p53 along with its binding partners have emerged as major determinants of its functional selectivity and specificity. Unravelling the intricacies of p53 functions have been augmented with the development of new mouse models of p53, which also have been discussed in this review.

引用

页码：786 / 794

页数：9

共 106 条

[21] E1A signaling to p53 involves the p19ARF tumor suppressor [J].

de Stanchina, E ;

McCurrach, ME ;

Zindy, F ;

Shieh, SY ;

Ferbeyre, G ;

Samuelson, AV ;

Prives, C ;

Roussel, MF ;

Sherr, CJ ;

Lowe, SW .

GENES & DEVELOPMENT, 1998, 12 (15) :2434-2442

[22] Regulation of a senescence checkpoint response by the E2F1 transcription factor and p14ARF tumor suppressor [J].

Dimri, GP ;

Itahana, K ;

Acosta, M ;

Campisi, J .

MOLECULAR AND CELLULAR BIOLOGY, 2000, 20 (01) :273-285

[23]

DOMAN D, 2004, NATURE, V429, P86

[24] MICE DEFICIENT FOR P53 ARE DEVELOPMENTALLY NORMAL BUT SUSCEPTIBLE TO SPONTANEOUS TUMORS [J].

DONEHOWER, LA ;

HARVEY, M ;

SLAGLE, BL ;

MCARTHUR, MJ ;

MONTGOMERY, CA ;

BUTEL, JS ;

BRADLEY, A .

NATURE, 1992, 356 (6366) :215-221

[25] Serine15 phosphorylation stimulates p53 transactivation but does not directly influence interaction with HDM2 [J].

Dumaz, N ;

Meek, DW .

EMBO JOURNAL, 1999, 18 (24) :7002-7010

[26] DEFINITION OF A CONSENSUS BINDING-SITE FOR P53 [J].

ELDEIRY, WS ;

KERN, SE ;

PIETENPOL, JA ;

KINZLER, KW ;

VOGELSTEIN, B .

NATURE GENETICS, 1992, 1 (01) :45-49

[27] WAF1, A POTENTIAL MEDIATOR OF P53 TUMOR SUPPRESSION [J].

ELDEIRY, WS ;

TOKINO, T ;

VELCULESCU, VE ;

LEVY, DB ;

PARSONS, R ;

TRENT, JM ;

LIN, D ;

MERCER, WE ;

KINZLER, KW ;

VOGELSTEIN, B .

CELL, 1993, 75 (04) :817-825

[28] PRESENCE OF A POTENT TRANSCRIPTION ACTIVATING SEQUENCE IN THE P53 PROTEIN [J].

FIELDS, S ;

JANG, SK .

SCIENCE, 1990, 249 (4972) :1046-1049

[29] Potentially important microRNA cluster on chromosome 17p13.1 in primary peritoneal carcinoma [J].

Flavin, Richard J. ;

Smyth, Paul C. ;

Laios, Alexandros ;

O'Toole, Sharon A. ;

Barrett, Ciara ;

Finn, Stephen P. ;

Russell, Susan ;

Ring, Martina ;

Denning, Karen M. ;

Li, Jinghuan ;

Aherne, Sinead T. ;

Sammarae, Dania A. ;

Aziz, Natasha A. ;

Alhadi, Araibi ;

Sheppard, Brian L. ;

Lao, Kai ;

Sheils, Orla M. ;

O'Leary, John J. .

MODERN PATHOLOGY, 2009, 22 (02) :197-205

[30] Participation of the human p53 3'UTR in translational repression and activation following gamma-irradiation [J].

Fu, LN ;

Benchimol, S .

EMBO JOURNAL, 1997, 16 (13) :4117-4125

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