ArticleScience signaling2013
Inositol polyphosphate multikinase is a coactivator of p53-mediated transcription and cell death.
Article in Science signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 56 citations in OpenAlex.
- IPMK at the crossroads of cellular signaling in health and disease.FEBS letters · 2026Review
- The nuclear phosphoinositide-p53 signalosome in the regulation of cell motility.Protein & cell · 2025Review
- From Obscurity to Prominence: IPMK's Expanding Role in Cellular Signaling, Physiology, and Disease.Biomolecules · 2025Review
- Loss of Skeletal Muscle Inositol Polyphosphate Multikinase Disrupts Glucose Regulation and Limits Exercise Capacity.International journal of molecular sciences · 2025Article
- A non-catalytic role of IPMK is required for PLCγ1 activation in T cell receptor signaling by stabilizing the PLCγ1-Sam68 complex.Cell communication and signaling : CCS · 2024Article
- Arg1 frommBio · 2024Article
- Nuclear phosphoinositide signaling promotes YAP/TAZ-TEAD transcriptional activity in breast cancer.The EMBO journal · 2024Article
- Article
- miRNA-Induced Downregulation of IPMK in Macrophages Mediates Lipopolysaccharide-Triggered TLR4 Signaling.Biomolecules · 2023Article
- A p53-phosphoinositide signalosome regulates nuclear AKT activation.Nature cell biology · 2022Article
- Phosphorylation-dependent association of human chromatin protein PC4 to linker histone H1 regulates genome organization and transcription.Nucleic acids research · 2022Article
- Article
- When PIPFrontiers in cell and developmental biology · 2022Review
- Inositol Polyphosphate Multikinase Signaling: Multifaceted Functions in Health and Disease.Molecules and cells · 2021Review
- Myeloid IPMK promotes the resolution of serum transfer-induced arthritis in mice.Animal cells and systems · 2021Article
- Rice EARLY SENESCENCE 2, encoding an inositol polyphosphate kinase, is involved in leaf senescence.BMC plant biology · 2020Article
- The nuclear phosphoinositide response to stress.Cell cycle (Georgetown, Tex.) · 2020Review
- Structural analyses of inositol phosphate second messengers bound to signaling effector proteins.Advances in biological regulation · 2020Review
- Inositol polyphosphate multikinase mediates extinction of fear memory.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Inositol Polyphosphate Multikinase (Genes · 2019Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The tumor suppressor protein p53 is a critical stress response transcription factor that induces the expression of genes leading to cell cycle arrest, apoptosis, and tumor suppression. We found that mammalian inositol polyphosphate multikinase (IPMK) stimulated p53-mediated transcription by binding to p53 and enhancing its acetylation by the acetyltransferase p300 independently of its inositol phosphate and lipid kinase activities. Genetic or RNA interference (RNAi)-mediated knockdown of IPMK resulted in decreased activation of p53, decreased recruitment of p53 and p300 to target gene promoters, abrogated transcription of p53 target genes, and enhanced cell viability. Additionally, blocking the IPMK-p53 interaction decreased the extent of p53-mediated transcription. These results suggest that IPMK acts as a transcriptional coactivator for p53 and that it is an integral part of the p53 transcriptional complex facilitating cell death.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.