Inositol Polyphosphate Multikinase Is a Coactivator of P53-Mediated Transcription and Cell Death
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By promoting p53 acetylation and activation, IPMK contributes to DNA damage–induced cell death.
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IPMK loss significantly impairs p53-mediated transcription in cell lines.
“Xu et al. [48] demonstrated that IPMK loss significantly impairs p53-mediated transcription in cell lines.”
From From Obscurity to Prominence: IPMK’s Expanding Role in Cellular Signaling, Physiology, and Disease (2025) · cites this paper as [48]
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Cites
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“IPMK is required for p53-mediated cell death As a tumor suppressor, p53 activates proapoptotic genes to induce cell death (41).”
Structure of Hdac3 Bound to Co-Repressor and Inositol Tetraphosphate
Watson, P. J., Fairall, L., Santos, G. M., & Schwabe, J. W. R. (2012) · Nature · doi:10.1038/nature10728 · Cited by 505 · cited 1× · see citing works
“(54) reported the crystal structure of histone deacetylase 3 and the activation domain of nuclear co-repressor 2, which requires the presence of the IPMK metabolite IP4 at the protein-protein Fig.”
A Role for Nuclear Inositol 1,4,5-Trisphosphate Kinase in Transcriptional Control
Odom, A. R., Stahlberg, A., Wente, S. R., & York, J. D. (2000) · Science · doi:10.1126/science.287.5460.2026 · Cited by 394 · see citing works
Modulation of ATP-Dependent Chromatin-Remodeling Complexes by Inositol Polyphosphates
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“Xu et al. [48] demonstrated that IPMK loss significantly impairs p53-mediated transcription in cell lines.”
- Authors
- Xu, R., Sen, N., Paul, B. D., Snowman, A. M., Rao, F., Vandiver, M. S., Xu, J., & Snyder, S. H.
- Affiliations
- Johns Hopkins University (US)
- Corresponding author
- Xu, Risheng
- Sen, Nilkantha
- Snyder, Solomon H.
- Venue
- Science Signaling
- Published
- 2013-04-02
- Volume
- 6
- Issue
- 269
- Pages
- ra22-ra22
- ISSN
- 1937-9145 (ISSN-L)
- 1945-0877
- PMC
- PMC4108196
- OpenAlex
- W2114706877
- Cited by
- 52
- References
- 9
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 3 · 2023: 2 · 2022: 4 · 2021: 2 · 2020: 2 · 2019: 5 · 2018: 2 · 2017: 6 · 2016: 5 · 2015: 6 · 2014: 5 · 2013: 4
- FWCI
- 3.57
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Signaling (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Drug Abuse (P50DA000266, DA000266)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- inositol polyphosphate multikinase, p53, transcriptional coactivator, P300, p53 acetylation, apoptosis, cell death, tumor suppression, transcriptional complex
- MeSH terms
- p300-CBP-Associated Factor, Acetylation, Animals, Antineoplastic Agents, Cell Survival, Cells, Cultured, Embryo, Mammalian, Etoposide, Fibroblasts, Humans, Promoter Regions, Genetic, Protein Binding, Proto-Oncogene Proteins, Transcription, Genetic, Blotting, Western, Trans-Activators, Tumor Suppressor Protein p53, Phosphotransferases (Alcohol Group Acceptor), Mice, Knockout, Reverse Transcriptase Polymerase Chain Reaction, RNA Interference, HCT116 Cells, Cell Line, Tumor, p300-CBP Transcription Factors, Apoptosis Regulatory Proteins, bcl-2-Associated X Protein, Mice
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