ArticleProceedings of the National Academy of Sciences of the United States of America2022
Inositol hexakisphosphate kinase-2 non-catalytically regulates mitophagy by attenuating PINK1 signaling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 21 citations in OpenAlex.
- Eating Disorders and Parkinson's Disease-2: Genetic Epidemiology and Shared Genomics.European eating disorders review : the journal of the Eating Disorders Association · 2026Article
- Inositol pyrophosphate kinases in health and disease.FEBS letters · 2026Review
- Eating Disorders and Parkinson's Disease - 2: Population Burden, Genetic Epidemiology and Shared Genomics.medRxiv : the preprint server for health sciences · 2026Article
- Clinical progression and genetic pathways in body-first and brain-first Parkinson's disease.Molecular neurodegeneration · 2025Article
- Knockout Mice as an Experimental Model to Study the Biology of Inositol Pyrophosphates.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Shared genetic architecture and bidirectional clinical risks within the psycho-metabolic nexus.EBioMedicine · 2025Article
- Machine learning nominates the inositol pathway and novel genes in Parkinson's disease.Brain : a journal of neurology · 2024Article
- Unraveling the Genetic Landscape of Neurological Disorders: Insights into Pathogenesis, Techniques for Variant Identification, and Therapeutic Approaches.International journal of molecular sciences · 2024Review
- Functions, Mechanisms, and therapeutic applications of the inositol pyrophosphates 5PP-InsPJournal of cardiovascular translational research · 2024Review
- Assessment tools for cognitive performance in Parkinson's disease and its genetic contributors.Frontiers in neurology · 2024Article
- Article
- The Role of Inositol Hexakisphosphate Kinase in the Central Nervous System.Biomolecules · 2023Review
- Investigation of enzalutamide, docetaxel, and cabazitaxel resistance in the castration resistant prostate cancer cell line C4 using genome-wide CRISPR/Cas9 screening.Scientific reports · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Inositol pyrophosphates, such as 5-diphosphoinositol pentakisphosphate (IP7), are generated by a family of inositol hexakisphosphate kinases (IP6Ks), of which IP6K2 has been implicated in various cellular functions including neuroprotection. Absence of IP6K2 causes impairment of oxidative phosphorylation regulated by creatine kinase-B. In the present study, we show that IP6K2 is involved in attenuation of PINK1-mediated mitochondrial autophagy (mitophagy) in the brain. Up-regulation of dynamin-related protein (Drp-1), as well as increased expression of mitochondrial biogenesis markers (PGC1-α and NRF-1) in the cerebella of IP6K2-deleted mice (IP6K2-knockout), point to the involvement of IP6K2 in the regulation of mitochondrial fission. Knockdown of IP6K2 also leads to augmented glycolysis, potentially as a compensatory mechanism for decreased mitochondrial respiration. Overexpressing IP6K2 as well as IP6K2-kinase dead mutant in IP6K2-knockdown N2A cells reverses the expression of mitophagy markers, demonstrating that IP6K2-induced mitoprotection is catalytically/kinase independent. IP6K2 supplementation in K2-PINK1 double-knockdown N2A cells fails to reverse the expression of the mitophagic marker, LC3-II, indicating that the mitoprotective effect of IP6K2 is dependent on PINK1. Overall, our study reveals a key neuroprotective role of IP6K2 in the prevention of PINK1-mediated mitophagy in the brain.
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