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PMID: 18503775 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Review

Transcriptional inhibitors, p53 and apoptoss.

Biochimica et biophysica acta ·Vol. 1786 ·No. 2 ·2008-12-00 ·Pages 83-6

Gartel AL

Abstract

Transcriptional inhibitors (TI) repress global transcription and induce apoptosis. It has been suggested that induction of p53 is one of the hallmarks of global transcriptional repression. Two recent papers suggested that treatment of human cancer cells with TIs, leads to p53-dependent, transcription-independent or p53-dependent, transcription-dependent apoptosis. The latter mechanism is linked to the fact that TIs can be selective in their inhibitory effects thereby permitting transcription of some genes. However, the majority of other published data suggest that these drugs induce p53-independent apoptosis. In this article I discuss the mechanisms of TI-dependent cell death and the potential role of p53 in this process.

MeSH Terms
Apoptosis/drug effects Cyclin-Dependent Kinase Inhibitor Proteins/physiology Humans Models, Biological RNA Polymerase II/metabolism Transcription, Genetic/drug effects Tumor Suppressor Protein p53/physiology
Chemicals
Cyclin-Dependent Kinase Inhibitor Proteins Tumor Suppressor Protein p53 RNA Polymerase II
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Gartel Andrei L
Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA. agartel@uic.edu
Article Info
Journal
Biochimica et biophysica acta
Abbr.
Biochim Biophys Acta
ISSN
0006-3002
Published
2008-12-00
Epub
2008-00-08
Pages
83-6
Language
English
Region
Netherlands
NLM ID
0217513
Subset
IM
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