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New job for an old tool: PI3Kβ phosphorylates OGT to regulate acetyl-CoA in glioblastoma
Journal article   Peer reviewed

New job for an old tool: PI3Kβ phosphorylates OGT to regulate acetyl-CoA in glioblastoma

Riley G. Young, Nusaiba N. Ahmed and Mauricio J. Reginato
Trends in cell biology, v 35(5), pp 361-363
01 May 2025
PMID: 40246630
url
https://pmc.ncbi.nlm.nih.gov/articles/PMC12048205/View
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Abstract

acetyl-CoA acetylation ACLY glioblastoma HK1 kinase O-GlcNAc transferase PI3Kβ
Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta (PI3Kβ) is recognized for its role in cellular signaling as a lipid kinase. He and colleagues recently reported a non-canonical function of PI3Kβ where, under high glucose, it phosphorylates and activates O-GlcNAc transferase (OGT). This activation enhances ATP-citrate synthase (ACLY) O-GlcNAcylation, increasing acetyl-CoA production, fueling fatty acid metabolism and histone acetylation, and driving glioblastoma (GBM) growth. Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta (PI3Kβ) is recognized for its role in cellular signaling as a lipid kinase. He and colleagues recently reported a non-canonical function of PI3Kβ where, under high glucose, it phosphorylates and activates O-GlcNAc transferase (OGT). This activation enhances ATP-citrate synthase (ACLY) O-GlcNAcylation, increasing acetyl-CoA production, fueling fatty acid metabolism and histone acetylation, and driving glioblastoma (GBM) growth.

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Collaboration types
Domestic collaboration
Web of Science research areas
Cell Biology
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