ArticleProceedings of the National Academy of Sciences of the United States of America2014
Inositol hexakisphosphate kinase-1 mediates assembly/disassembly of the CRL4-signalosome complex to regulate DNA repair and cell death.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
- Arabidopsis inositol polyphosphate kinase activities regulate COP9 deneddylation functions in phosphate homeostasis.Journal of integrative plant biology · 2026Article
- Inositol pyrophosphate kinases in health and disease.FEBS letters · 2026Review
- Meis1 isoform diversity orchestrates neural progenitor differentiation by regulating ATOH1 degradation at distinct subcellular compartments.PLoS biology · 2026Article
- Versatile roles of inositol hexakisphosphate in the ubiquitin-proteasome system.Essays in biochemistry · 2025Review
- The Use of Grating-Coupled Interferometry to Study Inositol Pyrophosphate-Protein Interactions.Methods in molecular biology (Clifton, N.J.) · 2025Article
- MicroRNA analysis of porcine muscle tissue involved in phosphoinositol metabolism.Frontiers in veterinary science · 2025Article
- Interaction with IP6K1 supports pyrophosphorylation of substrate proteins by the inositol pyrophosphate 5-InsP7.Bioscience reports · 2024Article
- Insights into the roles of inositol hexakisphosphate kinase 1 (IP6K1) in mammalian cellular processes.The Journal of biological chemistry · 2024Review
- Functions, Mechanisms, and therapeutic applications of the inositol pyrophosphates 5PP-InsPJournal of cardiovascular translational research · 2024Review
- Inositol hexakisphosphate kinases differentially regulate trafficking of vesicular glutamate transporters 1 and 2.Frontiers in cellular neuroscience · 2022Article
- Deletion of IP6K1 in mice accelerates tumor growth by dysregulating the tumor-immune microenvironment.Animal cells and systems · 2022Article
- DNA double strand break position leads to distinct gene expression changes and regulates VSG switching pathway choice.PLoS pathogens · 2021Article
- 5-IPNature metabolism · 2021Article
- MEKK1-Dependent Activation of the CRL4 Complex Is Important for DNA Damage-Induced Degradation of p21 and DDB2 and Cell Survival.Molecular and cellular biology · 2021Article
- Inositol phosphate kinases in the eukaryote landscape.Advances in biological regulation · 2021Article
- The Key Role of IPMolecules (Basel, Switzerland) · 2020Review
- Suramin and NF449 are IP5K inhibitors that disrupt inositol hexakisphosphate-mediated regulation of cullin-RING ligase and sensitize cancer cells to MLN4924/pevonedistat.The Journal of biological chemistry · 2020Article
- Inositol Pyrophosphates: Signaling Molecules with Pleiotropic Actions in Mammals.Molecules (Basel, Switzerland) · 2020Review
- Regulation of Cullin-RING E3 ligase dynamics by Inositol hexakisphosphate.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Targeting the Inositol Pyrophosphate Biosynthetic Enzymes in Metabolic Diseases.Molecules (Basel, Switzerland) · 2020Review
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Inositol polyphosphates containing an energetic pyrophosphate bond are formed primarily by a family of three inositol hexakisphosphate (IP6) kinases (IP6K1-3). The Cullin-RING ubiquitin ligases (CRLs) regulate diverse biological processes through substrate ubiquitylation. CRL4, comprising the scaffold Cullin 4A/B, the E2-interacting Roc1/2, and the adaptor protein damage-specific DNA-binding protein 1, is activated by DNA damage. Basal CRL4 activity is inhibited by binding to the COP9 signalosome (CSN). UV radiation and other stressors dissociate the complex, leading to E3 ligase activation, but signaling events that trigger signalosome dissociation from CRL4 have been unclear. In the present study, we show that, under basal conditions, IP6K1 forms a ternary complex with CSN and CRL4 in which IP6K1 and CRL4 are inactive. UV dissociates IP6K1 to generate IP7, which then dissociates CSN-CRL4 to activate CRL4. Thus, IP6K1 is a novel CRL4 subunit that transduces UV signals to mediate disassembly of the CRL4-CSN complex, thereby regulating nucleotide excision repair and cell death.
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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.