Cytoplasmic functions of the tumour suppressor p53
Open accessAbstract
The principal tumour-suppressor protein, p53, accumulates in cells in response to DNA damage, oncogene activation and other stresses. It acts as a nuclear transcription factor that transactivates genes involved in apoptosis, cell cycle regulation and numerous other processes. An emerging area of research unravels additional activities of p53 in the cytoplasm, where it triggers apoptosis and inhibits autophagy. These previously unknown functions contribute to the mission of p53 as a tumour suppressor.
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p53 protein can physically translocate to the mitochondria where it promotes membrane permeabilization and the release of the mitochondrial pro-apoptotic factors.
“In addition, p53 protein can physically translocate to the mitochondria where it promotes membrane permeabilization and the release of the mitochondrial pro-apoptotic factors(Green and Kroemer, 2009).”
From Programmed cell death in aging (2015) · cites this paper as Green and Kroemer, 2009
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- Authors
- Green, D. R., & Kroemer, G.
- Affiliations
- St. Jude Children's Research Hospital (US)
- Université Paris-Sud (FR)
- Corresponding author
- Green, Douglas R.
- Kroemer, Guido
- Venue
- Nature
- Published
- 2009-04
- Volume
- 458
- Issue
- 7242
- Pages
- 1127-1130
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC2814168
- OpenAlex
- W2059999514
- Cited by
- 1,106
- References
- 40
- Citations by year
- 2026: 17 · 2025: 34 · 2024: 37 · 2023: 69 · 2022: 51 · 2021: 51 · 2020: 54 · 2019: 57 · 2018: 62 · 2017: 59 · 2016: 88 · 2015: 74 · 2014: 69 · 2013: 93 · 2012: 91
- FWCI
- 8.46
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Institut National Du Cancer
- National Cancer Institute (P01CA069381)
- National Institute of General Medical Sciences (R37GM052735)
- National Institute of Allergy and Infectious Diseases (R01AI044828, R01AI040646, R01AI047891)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- p53, tumour suppressor, apoptosis, autophagy inhibition, DNA damage response, oncogene activation, transcription factors, cancer therapy targets
- MeSH terms
- Animals, Autophagy, Cell Nucleus, Cytoplasm, Humans, Mitochondria, Neoplasms, Transcription, Genetic, Tumor Suppressor Protein p53, Apoptosis
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