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, 2016; Cohen-Kaplan et al., 2017). While p62 principally carries out aggregation-dependent clearance of destroyed materials, p62 can flip detrimental by exacerbating pathological aggregation and proteotoxicity in the course of autophagy inhibition or when proteostasis is overcome. Considering the fact that p62 is an important receptor that provides substrates for both of those proteasomal degradation and autophagy, alterations in p62 degrees and performance could affect the exercise of UPS versus autophagy.
HDAC6 wants tubulin for trafficking, p62 accumulates if aggregates are not shipped to AP formation site
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The interactions of p62 as well as the UPS, autophagy and ubiquitinated proteins. On UPS inhibition, p62 is upregulated and phosphorylated on S405 and S409, which might aid the degradation of ubiquitinated cargoes via autophagy. p62 synthesis is induced by a rise in Nrf2 subsequent UPS deficiency. The enhanced p62 competes with Nrf2 for Keap1, and then a p62–Keap1 sophisticated selectively facilitates the ubiquitinated mixture development and generates a beneficial responses loop with Nrf2. HDAC6 can be activated because of the goods in UPS (which include K63), but inhibited straight by p62.
The S351 of KIR is phosphorylated, leading to a mounting affinity of p62 for Keap1 and followed by sequestration of Keap1 within the cargoes [seventy five].
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). Deletion of both equally p62 and Nrf2 spontaneously leads to the event of nonalcoholic steatohepatitis
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). DEPDC5 deficiency contributes to resistance to leucine starvation by way of p62 accumulation in hepatocellular carcinoma