ArticleApoptosis : an international journal on programmed cell death2026
PKCβ II antagonizes O-GlcNAcylated FOXO4 and inhibits lipid synthesis.
Article in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundObesity and associated metabolic disorders remain major public health challenges worldwide. The regulation of lipid synthesis represents a promising therapeutic target, yet the precise mechanisms remain elusive.
methodsRT-qPCR and western blot measured gene expression. Lipid droplets were evaluated by Nile Red staining. TC, HDL-C, LDL-C, TG and NEFA levels were detected by ELISA kits. The interaction between proteins or genes was analyzed by ChIP, Dual-luciferase reporter, and Co-IP assays. Subcellular localization was analyzed by nuclear/cytoplasmic fractionation and immunofluorescence.
resultsFOXO4 was downregulated after bariatric surgery and directly decreased the transcription of lipogenic enzymes ACACA and HMGCR. Nuclear localization of FOXO4 was regulated by a previously uncharacterized interplay between O-GlcNAcylation and phosphorylation. Specifically, O-GlcNAcylation at S261 promoted FOXO4 nuclear translocation and enhanced lipogenic gene expression, while PKCβII-mediated phosphorylation at T451 antagonized this modification. Functionally, FOXO4 deletion suppressed lipid synthesis under HFD conditions. OGA or PKCβII knockdown promoted lipid synthesis by regulating FOXO4.
conclusionElevated OGA inhibited FOXO4's nuclear translocation via O-GlcNAcylation, and subsequent PKCβII-mediated phosphorylation-induced degradation. This process decreased ACACA and HMGCR expression, thereby attenuating lipid synthesis.
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