The DOI matches its Crossref record; 93 of the 93 references it cites were found in a registry or an index.
Apoptosis - the p53 network
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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“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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1 retracted
RETRACTED: Regulation of p53: intricate loops and delicate balances
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RetractedApoptosis: A Basic Biological Phenomenon with Wideranging Implications in Tissue Kinetics
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“Indeed, approximately 50% of human cancers bear p53 gene mutations; in the majority of the remaining cancer cases, p53 activity is compromised by alternative mechanisms (Vogelstein et al., 2000).”
BackgroundDeath Receptors: Signaling and Modulation
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The Bcl-2 Protein Family: Arbiters of Cell Survival
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Cleavage of BID by Caspase 8 Mediates the Mitochondrial Damage in the Fas Pathway of Apoptosis
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A model for p53-induced apoptosis
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Ayala, A., Muñoz, M., & Argüelles, S. (2014) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2014/360438 · Cited by 6,837
Mitochondrial membrane permeabilization in cell death
Kroemer, G., Galluzzi, L., & Brenner, C. (2007) · Physiological Reviews · doi:10.1152/physrev.00013.2006 · Cited by 3,598
Pistritto, G., Trisciuoglio, D., Ceci, C., Garufi, A., & D’Orazi, G. (2016) · Aging · doi:10.18632/aging.100934 · Cited by 1,721
Physiology of cell volume regulation in vertebrates
Hoffmann, E. K., Lambert, I. H., & Pedersen, S. F. (2009) · Physiological Reviews · doi:10.1152/physrev.00037.2007 · Cited by 1,441
Census and evaluation of p53 target genes
Fischer, M. (2017) · Oncogene · doi:10.1038/onc.2016.502 · Cited by 971
Metadata
- Authors
- Haupt, S., Berger, M., Goldberg, Z., & Haupt, Y.
- Affiliations
- Hebrew University of Jerusalem (IL)
- Corresponding author
- Haupt, Ygal
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- 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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