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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Sies, Helmut / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred

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IMPACT FACTOR 2016: 3.273

CiteScore 2016: 3.01

SCImago Journal Rank (SJR) 2016: 1.679
Source Normalized Impact per Paper (SNIP) 2016: 0.800

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1437-4315
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Volume 389, Issue 4

Issues

p53-dependent repression of the human MCL-1 gene encoding an anti-apoptotic member of the BCL-2 family: the role of Sp1 and of basic transcription factor binding sites in the MCL-1 promoter

Maciej Pietrzak
  • 1Department of Endocrinology, Medical Research Center, Polish Academy of Sciences, 02-106 Warsaw, Poland
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Monika Puzianowska-Kuznicka
  • 2Department of Endocrinology, Medical Research Center, Polish Academy of Sciences, 02-106 Warsaw, Poland and Department of Biochemistry and Molecular Biology, Medical Center of Postgraduate Education, 01-813 Warsaw, Poland
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
Published Online: 2008-03-27 | DOI: https://doi.org/10.1515/BC.2008.039

Abstract

p53 regulates transcription of one anti-apoptotic and four pro-apoptotic members of the BCL-2 family, but nothing is known about the regulation of MCL-1, another anti-apoptotic member of this family, by p53. Confocal microscopic analysis of COS1, HEK 293 and HeLa cells transfected with a p53 expression plasmid demonstrated a decrease in the signal of endogenous MCL-1 compared to neighboring non-transfected cells. Transcription regulation assays showed that the 1826 bp human MCL-1 promoter fragment was repressed up to 30-fold by wild-type p53 in a dose-dependent manner. As shown by electrophoretic mobility shift assays, Sp1 binding to the sites located in the -295 to +16 MCL-1 promoter fragment was decreased in the presence of p53. However, the MCL-1 promoter devoid of all Sp1 binding sites was still repressed by p53, albeit 2-fold weaker than the wild-type promoter. Overexpression of Sp1 reduced p53-dependent repression of the MCL-1 promoter only up to 2.2-fold. Transcription regulation assays performed with MCL-1 promoter deletion mutants showed that most of the p53 inhibitory effect was mediated by the -41 to +16 bp promoter fragment containing binding sites only for TATA-binding protein and other basal transcription factors. We propose a novel, promoter-based mechanism by which p53 down-regulates expression of the anti-apoptotic MCL-1 protein.

Keywords: basal transcription factors; gene repression; MCL-1; Sp1; wild-type and mutant p53

About the article

Corresponding author


Received: 2007-10-19

Accepted: 2008-01-08

Published Online: 2008-03-27

Published in Print: 2008-04-01


Citation Information: Biological Chemistry, Volume 389, Issue 4, Pages 383–393, ISSN (Online) 14374315, ISSN (Print) 14316730, DOI: https://doi.org/10.1515/BC.2008.039.

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