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When Poldip2 is deficient, it induces protein O-GlcNAcylation and inhibits the ubiquitin-proteasome system through metabolic reprogramming (TCA cycle inhibition, glycolytic activity, increased HBP activity), resulting in the accumulation of polyubiquitinated proteins in the nucleus to maintain the stability of SRF, ultimately leading to VSMC differentiation [136]

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These exon transcripts have yet to be characterized and future proteomic studies may reveal their biological importance