Deacetylation of p53 induces autophagy by suppressing Bmf expression
Open accessAbstract
Interferon γ (IFN-γ)-induced cell death is mediated by the BH3-only domain protein, Bik, in a p53-independent manner. However, the effect of IFN-γ on p53 and how this affects autophagy have not been reported. The present study demonstrates that IFN-γ down-regulated expression of the BH3 domain-only protein, Bmf, in human and mouse airway epithelial cells in a p53-dependent manner. p53 also suppressed Bmf expression in response to other cell death-stimulating agents, including ultraviolet radiation and histone deacetylase inhibitors. IFN-γ did not affect Bmf messenger RNA half-life but increased nuclear p53 levels and the interaction of p53 with the Bmf promoter. IFN-γ-induced interaction of HDAC1 and p53 resulted in the deacetylation of p53 and suppression of Bmf expression independent of p53's proline-rich domain. Suppression of Bmf facilitated IFN-γ-induced autophagy by reducing the interaction of Beclin-1 and Bcl-2. Furthermore, autophagy was prominent in cultured bmf(-/-) but not in bmf(+/+) cells. Collectively, these observations show that deacetylation of p53 suppresses Bmf expression and facilitates autophagy.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
HDAC1/2 multiprotein complexes can also repress the expression of pro-apoptotic genes.
“Focusing on a single target gene could lead to misinterpretation, as HDAC1/2 multiprotein complexes can also repress the expression of pro-apoptotic genes (Contreras et al., 2013;Piazza et al., 2013;Ramsey, He, Forster, Ory, & Ellisen, 2011).”
From HDACs and the epigenetic plasticity of cancer cells: target the complexity (2022) · cites this paper as Contreras et al., 2013
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 59 · Cited by 48
Research works printed but not linked: 1
- Tesfaigzi Y. Fischer M.J. Daheshia M. Green F.H. De Sanctis G.T. Wilder J.A. 2002b Bax is crucial for IFN-γ-induced resolution of allergen-induced mucus cell metaplasia. J. Immunol. 169: 5919– 5925 12421976
- Authors
- Contreras, A. U., Mebratu, Y., Delgado, M., Montano, G., Hu, C.-A. A., Ryter, S. W., Choi, A. M. K., Lin, Y., Xiang, J., Chand, H., & Tesfaigzi, Y.
- Affiliations
- Lovelace Respiratory Research Institute (US)
- Chronic Obstructive Pulmonary Disease Program, Lovelace Respiratory Research Institute, Albuquerque, NM 87108 1
- University of New Mexico (US)
- Brigham and Women's Hospital (US)
- Illinois Institute of Technology, Chicago, IL 60616 4
- Illinois Institute of Technology (US)
- Corresponding author
- Tesfaigzi, Yohannes
- ORCID
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2013-04-29
- Volume
- 201
- Issue
- 3
- Pages
- 427-437
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC3639396
- OpenAlex
- W2156948821
- Cited by
- 48
- References
- 59
- Citations by year
- 2026: 2 · 2025: 3 · 2023: 1 · 2022: 5 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 5 · 2017: 3 · 2016: 7 · 2015: 6 · 2014: 9 · 2013: 3
- FWCI
- 6.31
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- National Institutes of Health (5r01hl068111-18)
- National Heart, Lung, and Blood Institute (R01-HL068111, R56HL068111, HL068111, P01HL114501)
- National Institute of Environmental Health Sciences (R01ES015482, ES015482)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- p53 deacetylation, autophagy, BMF, interferon-gamma, BH3-only proteins, HDAC1, Beclin-1, Bcl-2, airway epithelial cells, histone deacetylase inhibitors, ultraviolet radiation, p53 transcriptional regulation, cell death
- MeSH terms
- Acetylation, Animals, Autophagy, Cell Nucleus, Cells, Cultured, Epithelial Cells, Humans, Hydroxamic Acids, Interferon-gamma, Mice, Inbred C57BL, Promoter Regions, Genetic, Protein Processing, Post-Translational, Gene Expression, Tumor Suppressor Protein p53, Mice, Knockout, Butyric Acid, Respiratory Mucosa, Gene Silencing, Adaptor Proteins, Signal Transducing, Mice, Histone Deacetylase 1, Histone Deacetylase Inhibitors, Mice, 129 Strain
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
