Literature DB >> 8791489

p53 in signaling checkpoint arrest or apoptosis.

S Bates1, K H Vousden.   

Abstract

The cell cycle arrest and apoptotic functions of p53 both contribute to the role of this tumour suppressor protein in preventing replication of cells suffering DNA damage. Although the ability of p53 to function as a sequence-specific transcription factor appears to be directly and causally linked to the implementation of an arrest at the G1 stage of the cell cycle, the contribution of transcriptional activation to the apoptotic response is less clear. It seems likely that several p53 activities, both transcriptionally dependent and transcriptionally independent, can play a role in mediating cell death. The requirement for each of these functions appears to depend on the cell type, the cell environment and other genetic alterations already sustained by the cell in which p53 function is activated.

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Year:  1996        PMID: 8791489     DOI: 10.1016/s0959-437x(96)90004-0

Source DB:  PubMed          Journal:  Curr Opin Genet Dev        ISSN: 0959-437X            Impact factor:   5.578


  75 in total

1.  T cell receptor-induced activation and apoptosis in cycling human T cells occur throughout the cell cycle.

Authors:  M Karas; T Z Zaks; J L Liu; D LeRoith
Journal:  Mol Biol Cell       Date:  1999-12       Impact factor: 4.138

2.  AP-1 repressor protein JDP-2: inhibition of UV-mediated apoptosis through p53 down-regulation.

Authors:  F Piu; A Aronheim; S Katz; M Karin
Journal:  Mol Cell Biol       Date:  2001-05       Impact factor: 4.272

3.  Middle T antigen activation of signal transduction pathways does not overcome p53-mediated growth arrest.

Authors:  J Doherty; R Freund
Journal:  J Virol       Date:  1999-09       Impact factor: 5.103

4.  Stress signals utilize multiple pathways to stabilize p53.

Authors:  M Ashcroft; Y Taya; K H Vousden
Journal:  Mol Cell Biol       Date:  2000-05       Impact factor: 4.272

5.  The involvement of p53 in dopamine-induced apoptosis of cerebellar granule neurons and leukemic cells overexpressing p53.

Authors:  D Daily; A Barzilai; D Offen; A Kamsler; E Melamed; I Ziv
Journal:  Cell Mol Neurobiol       Date:  1999-04       Impact factor: 5.046

6.  mtCLIC/CLIC4, an organellular chloride channel protein, is increased by DNA damage and participates in the apoptotic response to p53.

Authors:  Ester Fernández-Salas; Kwang S Suh; Vladislav V Speransky; Wendy L Bowers; Joshua M Levy; Tracey Adams; Kamal R Pathak; Lindsay E Edwards; Daniel D Hayes; Christina Cheng; Alasdair C Steven; Wendy C Weinberg; Stuart H Yuspa
Journal:  Mol Cell Biol       Date:  2002-06       Impact factor: 4.272

Review 7.  p53-dependent cell death signaling in neurons.

Authors:  Richard S Morrison; Yoshito Kinoshita; Mark D Johnson; Weiqun Guo; Gwenn A Garden
Journal:  Neurochem Res       Date:  2003-01       Impact factor: 3.996

8.  Hydrogen peroxide-induced apoptosis in human hepatoma cells is mediated by CD95(APO-1/Fas) receptor/ligand system and may involve activation of wild-type p53.

Authors:  C Huang; J Li; R Zheng; K Cui
Journal:  Mol Biol Rep       Date:  2000-03       Impact factor: 2.316

9.  The hepatitis B virus X gene induces p53-mediated programmed cell death.

Authors:  P Chirillo; S Pagano; G Natoli; P L Puri; V L Burgio; C Balsano; M Levrero
Journal:  Proc Natl Acad Sci U S A       Date:  1997-07-22       Impact factor: 11.205

10.  Driving p53 response to Bax activation greatly enhances sensitivity to taxol by inducing massive apoptosis.

Authors:  P De Feudis; S Vignati; C Rossi; T Mincioni; R Giavazzi; M D'Incalci; M Broggini
Journal:  Neoplasia       Date:  2000 May-Jun       Impact factor: 5.715

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