Literature DB >> 8479742

Wild-type but not mutant p53 can repress transcription initiation in vitro by interfering with the binding of basal transcription factors to the TATA motif.

N Ragimov1, A Krauskopf, N Navot, V Rotter, M Oren, Y Aloni.   

Abstract

It has previously been shown that excess wild type (wt) p53 can repress the transcriptional activity of a variety of promoters in intact cells. To determine whether this transcriptional repression represented a direct effect of p53, wt and mutant p53 were prepared from E. coli-produced p53 and from insect cells infected with a recombinant baculovirus. When added into an in vitro transcription system, wt p53, but not mutant p53 reduced markedly transcription from the c-myc promoter, as well as from an array of other promoters, with the exception of an MHC class I gene promoter. The presence of wt p53 seemed to affect specifically the formation of the transcription preinitiation complex because preformed initiation complexes were completely refractory to wt p53, as was also the process of transcript elongation. Wild-type but not mutant p53 interfered with the stable binding of TBP and TFIIA to the TATA motif, although both wt and mutant p53 could associate in vitro with purified TBP. We propose that upon binding to TBP, wt but not mutant p53 specifically blocks the ability of TBP to engage in interactions required for efficient transcriptional initiation. This may account, at least in part, for the ability of excess wt p53 to inhibit cell proliferation and to interfere with neoplastic processes.

Entities:  

Mesh:

Substances:

Year:  1993        PMID: 8479742

Source DB:  PubMed          Journal:  Oncogene        ISSN: 0950-9232            Impact factor:   9.867


  57 in total

1.  The tumor suppressor p53 inhibits Net, an effector of Ras/extracellular signal-regulated kinase signaling.

Authors:  Koji Nakade; Hong Zheng; Gitali Ganguli; Gilles Buchwalter; Christian Gross; Bohdan Wasylyk
Journal:  Mol Cell Biol       Date:  2004-02       Impact factor: 4.272

2.  Transcriptional repression by p53 involves molecular interactions distinct from those with the TATA box binding protein.

Authors:  G Farmer; P Friedlander; J Colgan; J L Manley; C Prives
Journal:  Nucleic Acids Res       Date:  1996-11-01       Impact factor: 16.971

3.  Exonucleolytic degradation of RNA by p53 protein in cytoplasm.

Authors:  Mary Bakhanashvili; Rachel Gedelovich; Shai Grinberg; Galia Rahav
Journal:  J Mol Med (Berl)       Date:  2007-08-15       Impact factor: 4.599

4.  Distinct roles for p107 and p130 in Rb-independent cellular senescence.

Authors:  Brian D Lehmann; Adam M Brooks; Matthew S Paine; William H Chappell; James A McCubrey; David M Terrian
Journal:  Cell Cycle       Date:  2008-03-07       Impact factor: 4.534

5.  Dual inactivation of RB and p53 pathways in RAS-induced melanomas.

Authors:  N Bardeesy; B C Bastian; A Hezel; D Pinkel; R A DePinho; L Chin
Journal:  Mol Cell Biol       Date:  2001-03       Impact factor: 4.272

6.  p53 is a general repressor of RNA polymerase III transcription.

Authors:  C A Cairns; R J White
Journal:  EMBO J       Date:  1998-06-01       Impact factor: 11.598

Review 7.  Expression of the stress-associated protein p8 is a requisite for tumor development.

Authors:  Juan L Iovanna
Journal:  Int J Gastrointest Cancer       Date:  2002

8.  Differential regulation of plasminogen activator and inhibitor gene transcription by the tumor suppressor p53.

Authors:  C Kunz; S Pebler; J Otte; D von der Ahe
Journal:  Nucleic Acids Res       Date:  1995-09-25       Impact factor: 16.971

9.  p53-Dependent transcriptional repression of c-myc is required for G1 cell cycle arrest.

Authors:  Jenny S L Ho; Weili Ma; Daniel Y L Mao; Samuel Benchimol
Journal:  Mol Cell Biol       Date:  2005-09       Impact factor: 4.272

10.  CMV promoter is repressed by p53 and activated by JNK pathway.

Authors:  Marianna Rodova; Renuka Jayini; Reddy Singasani; Elizabeth Chipps; M Rafiq Islam
Journal:  Plasmid       Date:  2013-02-01       Impact factor: 3.466

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.