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27-OH induced autophagy is dependent on the relation between nuclear factor erythroid 2 p45-related factor 2 (Nrf2)-dependent antioxidant response and p62.
our results showed that high CD44 (show CD44 Proteins) led to p62 (show GTF2H1 Proteins)-associated NRF2 (show GABPA Proteins) activation in CD44 (show CD44 Proteins)(high) breast CSC-like cells. NRF2 (show GABPA Proteins) activation contributed to the aggressive phenotype, tumor growth, and anticancer drug resistance of CD44 (show CD44 Proteins)(high) CSCs
results suggested that p62 plays a protective role in adipogenesis of human adipose-derived stromal cells through regulating mitophagy.
The results of the present study demonstrated that p62 may aggravate LPSinduced acute kidney injury in mice by promoting apoptosis in renal tubular epithelial cells.
Study supports HuR's role as an upstream regulator of p62 expression in ARPE-19 cells, helps to understand better the early events in response to a proautophagy stimulus.
Therefore in this review we discuss the role of p62 in autophagy, apoptosis and cancer through its different domains and outline the importance of modulating cellular levels of p62 in cancer therapeutics.
Both the metastatic and recurrent tumor tissues expressed less p62 than the patient-matched primary tumor. A significant inverse correlation has been found between p62 expression and both the disease-free survival and overall survival.
p62 deficiency in stromal fibroblasts promotes resistance to glutamine deprivation by the direct control of ATF4 stability through its p62-mediated polyubiquitination.
AGG is also found to trigger ubiquitination of PUMA which in turn interacted with p62 for prompting mitophagy suggesting that AGG turns on PUMA-mediated mitophagy in U87MG cells in both p62-dependent as well as in p62-independent manner
The results suggest that p62 may be an effective predictor of prognosis and a potential target for therapy in osteosarcoma.
These results suggest that overexpression of SQSTM1 in SOD1 (show SOD1 Proteins) (H46R) mice accelerates disease onset by compromising the protein degradation pathways.
these results suggested that trehalose can function as a novel activator of the p62 (show GTF2H1 Proteins)-Keap1 (show KEAP1 Proteins)/Nrf2 (show NFE2L2 Proteins) pathway, in addition to inducing autophagy. Therefore, trehalose may be useful to treat many chronic diseases involving oxidative stress and dysfunction of autophagy.
The studies findings imply that p62 signaling plays a crucial role in suppressing inflammatory cytokine production by globular adiponectin in macrophages.
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 (show INS Proteins).
Deletion of both p62/Sqstm1 and Nrf2 (show NFE2L2 Proteins) genes spontaneously leads to the development of NASH (show SAMSN1 Proteins).
p62 serves to prevent endoplasmic reticulum stress in mouse hypothalamus by maintaining protein folding capacity
The p62 (show GTF2H1 Proteins)-keap1 (show KEAP1 Proteins)-Nrf2 (show NFE2L2 Proteins) antioxidant pathway was primarily activated in the early stage of APAP hepatotoxicity.
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.
analysis of soluble SQSTM1 complexes and soluble complexes formed between SQSTM1 oligomers and LC3 (show MAP1LC3A Proteins) using a combination of fluorescence microscopy-based biophysical approaches in living cells
ENC1 (show ENC1 Proteins) interacts with the phosphorylated p62 (show GTF2H1 Proteins) to impair autophagic degradation of mutant huntingtin (show HTT Proteins) protein aggregates.
Loss-of-function of SQSTM1 may cause phenotypic features characterized by locomotor deficits and motor neuron axonal defects that are associated with a misregulation of autophagic processes.
This gene encodes a multifunctional protein that binds ubiquitin and regulates activation of the nuclear factor kappa-B (NF-kB) signaling pathway. The protein functions as a scaffolding/adaptor protein in concert with TNF receptor-associated factor 6 to mediate activation of NF-kB in response to upstream signals. Alternatively spliced transcript variants encoding either the same or different isoforms have been identified for this gene. Mutations in this gene result in sporadic and familial Paget disease of bone.
, sqstm1 protein
, EBI3-associated protein of 60 kDa
, EBI3-associated protein p60
, oxidative stress induced like
, phosphotyrosine independent ligand for the Lck SH2 domain p62
, phosphotyrosine-independent ligand for the Lck SH2 domain of 62 kDa
, ubiquitin-binding protein p62
, oxidative stress induced
, PKC-zeta-interacting protein
, protein kinase C-zeta-interacting protein