Back to article: Attenuating MKRN1 E3 ligase-mediated AMPKα suppression increases tolerance against metabolic stresses in mice

FIGURE 2: Targets of MKRN1. MKRN1 mediates the ubiquitination of AMPKα, p14ARF, p53, FADD, PTEN, and APC, which are then degraded via the proteasome-dependent pathway. AMPK, the energy sensor inducing catabolism, is also an activator of p53, which in turn enforces the function of PTEN, APC, and FADD via direct or indirect regulation. In particular, induction of PTEN by p53 leads to the suppression of AKT and thus of mTOR pathways, inhibiting the anabolic pathways. Thus, MKRN1 might have comprehensive effects on general metabolic pathways by regulating the factors involved.

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