Cited by 4,063Cancer-related Molecular PathwaysCell death mechanisms and regulationHeat shock proteins research

Tumor suppressor p53 is a direct transcriptional activator of the human bax gene

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Toshiyuki, Miyashita, Reed, John C·1995·Cell

Abstract

The bax gene promoter region contains four motifs with homology to consensus p53-binding sites. In cotransfection assays using p53-deficient tumor cell lines, wild-type but not mutant p53 expression plasmids transactivated a reporter gene plasmid that utilized the bax gene promoter to drive transcription of chloramphenicol acetyltransferase. In addition, wild-type p53 transactivated reporter gene constructs containing a heterologous minimal promoter and a 39-bp region from the bax gene promoter in which the p53-binding site consensus sequences reside. Introduction of mutations into the consensus p53-binding site sequences abolished p53 responsiveness of reporter gene plasmids. Wild-type but not mutant p53 protein bound to oligonucleotides corresponding to this region of the bax promoter, based on gel retardation assays. Taken together, the results suggest that bax is a p53 primary-response gene, presumably involved in a p53-regulated pathway for induction of apoptosis.

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Crossref · 10.1016/0092-8674(95)90412-3

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49 of 49 references verified0 citation errors · 0 not checkable

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  • Several proapoptotic BCL-2 family members, including BAX, BBC3 (PUMA) and PMAIP1 (NOXA), are activated by p53.

    “Several proapoptotic BCL-2 family members, including BAX,41, 42, 43 BBC3 (PUMA)181 and PMAIP1 (NOXA),182 are activated by p53.”

    From Census and evaluation of p53 target genes (2017) · cites this paper as [41]

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Authors
Toshiyuki, M., & Reed, J. C.
Affiliations
Sanford Burnham Prebys Medical Discovery Institute (US)
Venue
Cell
Publisher
Elsevier BV
Published
1995-01
Volume
80
Issue
2
Pages
293-299
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2045086385
Cited by
4,063
References
49
Citations by year
2026: 17 · 2025: 38 · 2024: 31 · 2023: 63 · 2022: 46 · 2021: 63 · 2020: 77 · 2019: 74 · 2018: 72 · 2017: 91 · 2016: 92 · 2015: 90 · 2014: 123 · 2013: 91 · 2012: 106
FWCI
87.27
Type
journal article
Language
en
Open access
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • American Cancer Society
  • National Institutes of Health (5r01ca060181-05)
  • National Cancer Institute (CA 60181)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
Keywords
p53, Bax gene, transcriptional activation, p53 binding sites, apoptosis, primary response genes, DNA binding
MeSH terms
Base Sequence, Binding Sites, Cell Line, Cosmids, Female, Humans, Molecular Sequence Data, Oligodeoxyribonucleotides, Placenta, Plasmids, Pregnancy, Promoter Regions, Genetic, Proto-Oncogene Proteins, Recombinant Proteins, Transfection, Restriction Mapping, Chloramphenicol O-Acetyltransferase, Transcriptional Activation, Gene Library, Gene Expression, Tumor Suppressor Protein p53, Mutagenesis, Consensus Sequence, Proto-Oncogene Proteins c-bcl-2, bcl-2-Associated X Protein

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