ArticleProceedings of the National Academy of Sciences of the United States of America2008
HSP90 regulates cell survival via inositol hexakisphosphate kinase-2.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 123 citations in OpenAlex.
- Inositol pyrophosphate kinases in health and disease.FEBS letters · 2026Review
- Targeting the Ip6k2-Runx2 axis disrupts osteoblast-osteoclast coupling to treat osteoporosis.Nature communications · 2026Article
- Anti-cancer properties of Sansalvamide A, its derivatives, and analogs: an updated review.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Identifying prognostic characteristics of m6A-related glycolysis gene and predicting the immune infiltration landscape in bladder cancer.Cancer cell international · 2023Article
- Article
- Ydj1 interaction at nucleotide-binding-domain of yeast Ssa1 impacts Hsp90 collaboration and client maturation.PLoS genetics · 2022Article
- Inositol hexakisphosphate kinase-2 non-catalytically regulates mitophagy by attenuating PINK1 signaling.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Leveraging Allele-Specific Expression for Therapeutic Response Gene Discovery in Glioblastoma.Cancer research · 2022Article
- Proteomic analysis reveals dual requirement for Grb2 and PLCγ1 interactions for BCR-FGFR1-Driven 8p11 cell proliferation.Oncotarget · 2022Article
- IP6K2 predicts favorable clinical outcome of primary breast cancer.Molecular and clinical oncology · 2021Article
- Multiple substrate recognition by yeast diadenosine and diphosphoinositol polyphosphate phosphohydrolase through phosphate clamping.Science advances · 2021Article
- PNSA, a Novel C-Terminal Inhibitor of HSP90, Reverses Epithelial-Mesenchymal Transition and Suppresses Metastasis of Breast Cancer Cells In Vitro.Marine drugs · 2021Article
- Inositol hexakisphosphate kinase-2 determines cellular energy dynamics by regulating creatine kinase-B.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Characterization of the dual functional effects of heat shock proteins (HSPs) in cancer hallmarks to aid development of HSP inhibitors.Genome medicine · 2020Article
- The Key Role of IPMolecules (Basel, Switzerland) · 2020Review
- Inositol hexakisphosphate kinase 2 promotes cell death of anterior horn cells in the spinal cord of patients with amyotrophic lateral sclerosis.Molecular biology reports · 2020Article
- Targeting the Inositol Pyrophosphate Biosynthetic Enzymes in Metabolic Diseases.Molecules (Basel, Switzerland) · 2020Review
- Synthesis and characterization of novel isoform-selective IP6K1 inhibitors.Bioorganic & medicinal chemistry letters · 2019Article
- Inositol Hexakisphosphate Kinase-2 in Cerebellar Granule Cells Regulates Purkinje Cells and Motor Coordination via Protein 4.1N.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Genomic regions underlying uniformity of yearling weight in Nellore cattle evaluated under different response variables.BMC genomics · 2018Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Heat-shock proteins (HSPs) are abundant, inducible proteins best known for their ability to maintain the conformation of proteins and to refold damaged proteins. Some HSPs, especially HSP90, can be antiapoptotic and the targets of anticancer drugs. Inositol hexakisphosphate kinase-2 (IP6K2), one of a family of enzymes generating the inositol pyrophosphate IP7 [diphosphoinositol pentakisphosphate (5-PP-IP5)], mediates apoptosis. Increased IP6K2 activity sensitizes cancer cells to stressors, whereas its depletion blocks cell death. We now show that HSP90 physiologically binds IP6K2 and inhibits its catalytic activity. Drugs and selective mutations that abolish HSP90-IP6K2 binding elicit activation of IP6K2, leading to cell death. Thus, the prosurvival actions of HSP90 reflect the inhibition of IP6K2, suggesting that selectively blocking this interaction could provide effective and safer modes of chemotherapy.
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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.