Cited by 1,136Cancer-related Molecular PathwaysCell death mechanisms and regulationHeat shock proteins research

Apoptosis - the p53 network

Haupt, Susan, Berger, Michael, Goldberg, Zehavit, Haupt, Ygal·2003·Journal of Cell Science

Abstract

Exposure to cellular stress can trigger the p53 tumor suppressor, a sequence-specific transcription factor, to induce cell growth arrest or apoptosis. The choice between these cellular responses is influenced by many factors, including the type of cell and stress, and the action of p53 co-activators. p53 stimulates a wide network of signals that act through two major apoptotic pathways. The extrinsic, death receptor pathway triggers the activation of a caspase cascade, and the intrinsic, mitochondrial pathway shifts the balance in the Bcl-2 family towards the pro-apoptotic members, promoting the formation of the apoptosome, and consequently caspase-mediated apoptosis. The impact of these two apoptotic pathways may be enhanced when they converge through Bid, which is a p53 target. The majority of these apoptotic effects are mediated through the induction of specific apoptotic target genes. However, p53 can also promote apoptosis by a transcription-independent mechanism under certain conditions. Thus, a multitude of mechanisms are employed by p53 to ensure efficient induction of apoptosis in a stage-, tissue- and stress-signal-specific manner. Manipulation of the apoptotic functions of p53 constitutes an attractive target for cancer therapy.

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Crossref · 10.1242/jcs.00739

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  • Apoptosis, both intrinsic and extrinsic, is induced via p53 target genes.

    “Apoptosis, both intrinsic and extrinsic, is induced via p53 target genes.176, 177”

    From Census and evaluation of p53 target genes (2017) · cites this paper as [176]

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Authors
Haupt, S., Berger, M., Goldberg, Z., & Haupt, Y.
Affiliations
Hebrew University of Jerusalem (IL)
Corresponding author
Haupt, Ygal
Venue
Journal of Cell Science
Published
2003-10-15
Volume
116
Issue
20
Pages
4077-4085
ISSN
  • 0021-9533 (ISSN-L)
  • 1477-9137
OpenAlex
W2103616303
Cited by
1,136
References
93
Citations by year
2026: 11 · 2025: 24 · 2024: 34 · 2023: 31 · 2022: 37 · 2021: 53 · 2020: 57 · 2019: 57 · 2018: 57 · 2017: 53 · 2016: 75 · 2015: 66 · 2014: 59 · 2013: 76 · 2012: 76
FWCI
3.47
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Cell Science (publishedVersion)
  • PubMed (publishedVersion)
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, apoptosis, p53 tumor suppressor, cellular stress response, growth arrest, death receptor signaling, mitochondrial apoptosis, Bcl-2 family proteins, apoptosome, caspase cascade, Bid, p53 target genes, cancer therapy
MeSH terms
Animals, Carrier Proteins, Cell Division, Enzyme Activation, Humans, Mitochondria, Proto-Oncogene Proteins, Signal Transduction, Tumor Suppressor Protein p53, Apoptosis, Protein Serine-Threonine Kinases, Proto-Oncogene Proteins c-bcl-2, Caspases, Protein Interaction Mapping, BH3 Interacting Domain Death Agonist Protein, Proto-Oncogene Proteins c-akt

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