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These results indicate that p62 predominantly suppresses murine in vitro osteoclast differentiation and highlight previously undetected Paget's disease-like phenotypes in p62(-/-) mice in vivo.
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the essential role that p62, particularly its PB1 and UBA domains, has in the formation of ALIS.
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Cereblon suppresses the formation of pathogenic protein aggregates in a p62-dependent manner.
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A complex of C9ORF72 and p62 uses arginine methylation to eliminate stress granules by autophagy.
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Atg7(f/f) Tyr-Cre mice, in which autophagy-related 7 (Atg7) is conditionally deleted under the control of the tyrosinase promoter, are a model for accumulations of the autophagy adapter and substrate sequestosome-1/p62 in both neuronal and neuroepithelial cells.
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These results suggest that overexpression of SQSTM1 in SOD1 (H46R) mice accelerates disease onset by compromising the protein degradation pathways.
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these results suggested that trehalose can function as a novel activator of the p62-Keap1/Nrf2 pathway, in addition to inducing autophagy. Therefore, trehalose may be useful to treat many chronic diseases involving oxidative stress and dysfunction of autophagy.
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The studies findings imply that p62 signaling plays a crucial role in suppressing inflammatory cytokine production by globular adiponectin in macrophages.
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Data, including data from studies in transgenic and knockout mice, suggest that p62/Sqstm1 is not required for normal pancreatic islet organization and beta-cell secretion of insulin.
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Deletion of both p62/Sqstm1 and Nrf2 genes spontaneously leads to the development of NASH.
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p62 serves to prevent endoplasmic reticulum stress in mouse hypothalamus by maintaining protein folding capacity
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The p62-keap1-Nrf2 antioxidant pathway was primarily activated in the early stage of APAP hepatotoxicity.
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Endogenous p62 undergoes E2-dependent ubiquitylation during upregulation of Ubiquitin (Ub) homeostasis, a condition termed as Ub(+) stress, that is intrinsic to Ub overexpression, heat shock or prolonged proteasomal inhibition by bortezomib, a chemotherapeutic drug.
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analysis of soluble SQSTM1 complexes and soluble complexes formed between SQSTM1 oligomers and LC3 using a combination of fluorescence microscopy-based biophysical approaches in living cells
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ENC1 interacts with the phosphorylated p62 to impair autophagic degradation of mutant huntingtin protein aggregates.
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this study proved that SYVN1 enhances SERPINA1(E342K)/ATZ degradation through SQSTM1-dependent autophagy and attenuates SERPINA1(E342K)/ATZ cytotoxicity.
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Data suggest that maternal nutrition modulates expression of autophagy proteins p62/Sqstm1 and Lc3-II/Map1lc3 in liver and hypothalamus of offspring (newborn, suckling, and adult stages); for example, high-fat diet leading to maternal obesity up-regulates p62 and down-regulates Lc3-II in neonatal liver. (p62/Sqstm1 = sequestosome 1; Lc3-II/Map1lc3 = microtubule-associated protein 1-light chain 3)
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TRIM11 suppresses AIM2 inflammasome by degrading AIM2 via p62-dependent selective autophagy.
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SQSTM1 dynamically associates with DNA damage foci (DDF) and regulates DNA repair.
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Thyroid hormone promotes selective autophagy via induction of DAPK2-SQSTM1 cascade, which in turn protects hepatocytes from diethylnitrosamine-induced hepatotoxicity or carcinogenesis.
