Cited by 110Cancer-related Molecular PathwaysGenomics and Chromatin DynamicsSignaling Pathways in Disease

p130/E2F4 Binds to and Represses the cdc2 Promoter in Response to p53

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Taylor, William R., Schönthal, Axel H., Galante, Jeanna, Stark, George R.·2001·Journal of Biological Chemistry

Abstract

p53 represses the transcription of cdc2 and cyclin B1, causing loss of Cdc2 activity and G(2) arrest. Here we show that the region -22 to -2 of the cdc2 promoter called the R box is required for repression by p53 but not for basal promoter activity. The R box confers p53-dependent repression on heterologous promoters and binds to p130/E2F4 in response to overexpression of p53. R box-dependent repression requires p21/waf1, and overexpression of p21/waf1 also represses the cdc2 promoter. These observations suggest that p53 represses the cdc2 promoter by inducing p21/waf1, which inhibits cyclin-dependent kinase activity, enhancing the binding of p130 and E2F4, which together bind to and repress the cdc2 promoter.

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Crossref · 10.1074/jbc.m005101200

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89 of 89 references verified0 citation errors · 0 not checkable

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  • p130 and E2F4 are recruited to cell cycle gene promoters when p21 is activated by p53.

    “Consistent with this notion, p130 and E2F4 are recruited to cell cycle gene promoters when p21 is activated by p53.98, 99”

    From Census and evaluation of p53 target genes (2017) · cites this paper as [98]

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Authors
Taylor, W. R., Schönthal, A. H., Galante, J., & Stark, G. R.
Affiliations
  • Cleveland Clinic (US)
  • University of Southern California (US)
Corresponding author
Stark, George R.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2001-01
Volume
276
Issue
3
Pages
1998-2006
ISSN
0021-9258 (ISSN-L)
OpenAlex
W2086565810
Cited by
110
References
89
Citations by year
2025: 2 · 2024: 1 · 2023: 3 · 2021: 1 · 2020: 3 · 2019: 2 · 2018: 1 · 2017: 3 · 2016: 4 · 2015: 2 · 2014: 2 · 2013: 2 · 2012: 2
FWCI
5.15
Type
journal article
Language
en
Open access
Locations
  • Journal of Biological Chemistry (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
National Institute of General Medical Sciences (GM49345, R01GM049345)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords
p53, transcriptional repression, p21, cyclin-dependent kinases, G2 cell cycle arrest, E2F4, cyclin B1
MeSH terms
Base Sequence, Cell Line, DNA, DNA-Binding Proteins, Molecular Sequence Data, Promoter Regions, Genetic, Protein Binding, Repressor Proteins, Transcription Factors, Transcription, Genetic, Tumor Suppressor Protein p53, Protein Serine-Threonine Kinases, Cyclin-Dependent Kinases, CDC2-CDC28 Kinases, E2F4 Transcription Factor, Cyclin-Dependent Kinase 2

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