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The authors show that ufmylation regulates SQSTM1 by eliciting a cell type-specific endoplasmic reticulum stress response which induces SQSTM1 expression and results in its accumulation in the cytosol.
TRIM11 suppresses AIM2 inflammasome by degrading AIM2 via p62-dependent selective autophagy.
These data define that YOD1 (Montrer YOD1 Kits ELISA) antagonizes TRAF6 (Montrer TRAF6 Kits ELISA)/p62 (Montrer GTF2H1 Kits ELISA)-dependent IL-1 (Montrer IL1A Kits ELISA) signaling to NF-kappaB (Montrer NFKB1 Kits ELISA).
Data show that p62 interaction with LC3, leading to the delivery of p62 and its cargoes to the autophagosome.
These results demonstrate a novel SQSTM1 regulatory network that promotes a nickel-induced tumorigenic effect in human bronchial epithelial cells.
Thyroid hormone (Montrer PTH Kits ELISA) promotes selective autophagy via induction of DAPK2 (Montrer DAPK2 Kits ELISA)-SQSTM1 cascade, which in turn protects hepatocytes from diethylnitrosamine-induced hepatotoxicity or carcinogenesis.
P62 functions as a tumour metastasis promoter.
Silence of p62 promotes apoptosis induced by mitochondrial depolarization.
Rare variants in SQSTM1 are risk for sporadic inclusion body myositis.
The WDR81 (Montrer WDR81 Kits ELISA) coordinates p62 (Montrer GTF2H1 Kits ELISA) and LC3C to facilitate autophagic removal of Ub proteins, and provide important insights into CAMRQ2 (Montrer WDR81 Kits ELISA) syndrome, a WDR81 (Montrer WDR81 Kits ELISA)-related developmental disorder.
SQSTM1 dynamically associates with DNA damage foci (DDF) and regulates DNA repair.
serine 351 phosphorylation of p62 (Montrer GTF2H1 Kits ELISA) did not enhance its binding to Keap1 (Montrer KEAP1 Kits ELISA) or stabilise the nuclear factor erythroid 2-related factor 2 (Nrf2 (Montrer NFE2L2 Kits ELISA)) transcription factor in this neuronal context. Nrf2 (Montrer NFE2L2 Kits ELISA) protein levels were markedly decreased despite transcriptional activation of the Nrf2 (Montrer NFE2L2 Kits ELISA) gene
Notch1-Hes-1 signaling controls TLR7-induced autophagic death of macrophage via regulation of P62 in mice with lupus.
Our findings show how p62 helps maintain intracellular pools of glutathione needed to limit mitochondrial dysfunction in tumor cells with elevated mTORC1
TRIM14 inhibits cGAS degradation mediated by selective autophagy receptor p62 to promote innate immune responses.
Authors found that p62/SQSTM1, a protein upregulated in liver parenchymal cells but downregulated in HCC (Montrer FAM126A Kits ELISA)-associated HSCs, negatively controls hepatic stellate cells activation.
SQSTM1 or damaged proteins may be transported from the nose to the brain. These findings strongly implicate widespread protein damage in the etiology of flavorings-related lung disease.
Promoting amino acid sensitivity of the mTOR pathway is dependent on p62 accumulation by inhibition of autophagy and this process plays an important role in the hepatic differentiation of stem/progenitor cells.
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