ArticleThe Journal of biological chemistry2009
Oxidative stress decreases phosphatidylinositol 4,5-bisphosphate levels by deactivating phosphatidylinositol- 4-phosphate 5-kinase beta in a Syk-dependent manner.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Targeting PIP5K ameliorates hepatic cancer by inhibiting PI3K/AKT and the autophagy mechanism and enhancing ROS-mediated apoptosis.Frontiers in pharmacology · 2026Article
- TMEM55A-mediated PI5P signalling regulates alpha cell actin depolymerisation and glucagon secretion.Diabetologia · 2025Article
- TMEM55A-mediated PI5P signaling regulates α-cell actin depolymerization and glucagon secretion.bioRxiv : the preprint server for biology · 2024Article
- Non-cell autonomous regulation of cell-cell signaling and differentiation by mitochondrial ROS.The Journal of cell biology · 2024Article
- Alzheimer's disease and cerebrovascular pathology alter inward rectifier potassium (KBritish journal of pharmacology · 2022Article
- When PIPFrontiers in cell and developmental biology · 2022Review
- Potential Interplay between Nrf2, TRPA1, and TRPV1 in Nutrients for the Control of COVID-19.International archives of allergy and immunology · 2021Review
- GABARAPs regulate PI4P-dependent autophagosome:lysosome fusion.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Reactive oxygen species in inflammation and tissue injury.Antioxidants & redox signaling · 2014Review
- Phosphoinositides: tiny lipids with giant impact on cell regulation.Physiological reviews · 2013Review
- Phosphatidylinositol-4-phosphate 5-kinase isoforms exhibit acyl chain selectivity for both substrate and lipid activator.The Journal of biological chemistry · 2012Article
- One lipid, multiple functions: how various pools of PI(4,5)P(2) are created in the plasma membrane.Cellular and molecular life sciences : CMLS · 2010Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Phosphatidylinositol 4,5-bisphosphate (PIP(2)) has many essential functions and its homeostasis is highly regulated. We previously found that hypertonic stress increases PIP(2) by selectively activating the beta isoform of the type I phosphatidylinositol phosphate 5-kinase (PIP5Kbeta) through Ser/Thr dephosphorylation and promoting its translocation to the plasma membrane. Here we report that hydrogen peroxide (H(2)O(2)) also induces PIP5Kbeta Ser/Thr dephosphorylation, but it has the opposite effect on PIP(2) homeostasis, PIP5Kbeta function, and the actin cytoskeleton. Brief H(2)O(2) treatments decrease cellular PIP(2) in a PIP5Kbeta-dependent manner. PIP5Kbeta is tyrosine phosphorylated, dissociates from the plasma membrane, and has decreased lipid kinase activity. In contrast, the other two PIP5K isoforms are not inhibited by H(2)O(2). We identified spleen tyrosine kinase (Syk), which is activated by oxidants, as a candidate PIP5Kbeta kinase in this pathway, and mapped the oxidant-sensitive tyrosine phosphorylation site to residue 105. The PIP5KbetaY105E phosphomimetic is catalytically inactive and cytosolic, whereas the Y105F non-phosphorylatable mutant has higher intrinsic lipid kinase activity and is much more membrane associated than wild type PIP5Kbeta. These results suggest that during oxidative stress, as modeled by H(2)O(2) treatment, Syk-dependent tyrosine phosphorylation of PIP5Kbeta is the dominant post-translational modification that is responsible for the decrease in cellular PIP(2).
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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.