IndraLab

Statements


OTUD4 activates PFKFB3. 4 / 4
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"Studies of post-myocardial infarction myocardial fibrosis revealed that OTU deubiquitinase 4 upregulated PFKFB3 to promote post-myocardial infarction cardiac fibrosis and that the inhibition of PFKFB3 helps ameliorate ischemia-induced cardiac fibrosis; therefore, the use of PFKFB3 inhibitors may provide a new therapeutic option for the treatment of post-myocardial infarction cardiac fibrosis (125)."

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"Deubiquitinase OTUD4 bonded to PFKFB3 and enhanced PFKFB3 stability via deubiquitylation upon TGF-β1 treatment."

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"OTUD4 promoted the stability of PFKFB3, leading to enhanced glycolysis and exacerbating cardiac fibrosis (Ref."

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"In addition, OTUD4 augments glycolysis by stabilizing glycolytic enzyme PFKFB3 in TGF-β1-treated cardiac fibroblasts and in cardiac fibroblasts of post-myocardial infarction mice [ 30 ]."