Transcription-independent pro-apoptotic functions of p53
Abstract
Induction of apoptosis is one of the central activities by which p53 exerts its tumor-suppressing function. Aside from its primary function as a transcription factor, it can promote apoptosis independent of transcription. Recent studies have started to define the mechanisms of non-transcriptional pro-apoptotic p53 activities operating within the intrinsic mitochondria-mediated pathway of apoptosis. So far, two different mechanisms have been described, each of which was assigned to a specific localization of the p53 protein, either in the cytosol or directly at the mitochondria. Although mechanistically different, both transcription-independent modes of apoptosis induction converge, as they both initiate permeabilization of the outer mitochondrial membrane via activation of the pro-apoptotic Bcl-2 family members Bax or Bak.
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The reduction of apoptosis by p53 knockdown is likely because the genetic inhibition nonspecifically altered a myriad of p53-related cellular functions, including induction of apoptosis.
“likely because the genetic inhibition nonspecifically altered a myriad of p53-related cellular functions, including induction of apoptosis (40).”
From <i>Txnip</i> Enhances Fitness of <i>Dnmt3a</i> -Mutant Hematopoietic Stem Cells via <i>p21</i> (2022) · cites this paper as [40]
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<i>Txnip</i> Enhances Fitness of <i>Dnmt3a</i> -Mutant Hematopoietic Stem Cells via <i>p21</i>
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- Authors
- Moll, U. M., Wolff, S., Speidel, D., & Deppert, W.
- Affiliations
- Stony Brook University (US)
- Leibniz Institute of Virology (LIV) (DE)
- Corresponding author
- Moll, Ute M
- Deppert, Wolfgang
- Venue
- Current Opinion in Cell Biology
- Publisher
- Elsevier BV
- Published
- 2005-12
- Volume
- 17
- Issue
- 6
- Pages
- 631-636
- ISSN
- 0955-0674 (ISSN-L)
- OpenAlex
- W2165997736
- Cited by
- 468
- References
- 4
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 6 · 2023: 13 · 2022: 9 · 2021: 13 · 2020: 7 · 2019: 23 · 2018: 11 · 2017: 17 · 2016: 27 · 2015: 22 · 2014: 27 · 2013: 35 · 2012: 32
- FWCI
- 3.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Philip Morris International
- National Institutes of Health
- National Cancer Institute (CA060664)
- 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, intrinsic mitochondrial apoptotic pathway, mitochondrial outer membrane permeabilization, Bax, Bak, Bcl-2 family proteins, mitochondrial p53, tumor suppression
- MeSH terms
- Cytosol, Humans, Nuclear Proteins, Transcription Factors, Tumor Suppressor Protein p53, Apoptosis, Mitochondrial Proteins
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