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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 (zeige YOD1 ELISA Kits) antagonizes TRAF6 (zeige TRAF6 ELISA Kits)/p62 (zeige GTF2H1 ELISA Kits)-dependent IL-1 (zeige IL1A ELISA Kits) signaling to NF-kappaB (zeige NFKB1 ELISA Kits).
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 (zeige PTH ELISA Kits) promotes selective autophagy via induction of DAPK2 (zeige DAPK2 ELISA Kits)-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 (zeige WDR81 ELISA Kits) coordinates p62 (zeige GTF2H1 ELISA Kits) and LC3C to facilitate autophagic removal of Ub proteins, and provide important insights into CAMRQ2 (zeige WDR81 ELISA Kits) syndrome, a WDR81 (zeige WDR81 ELISA Kits)-related developmental disorder.
SQSTM1 dynamically associates with DNA damage foci (DDF) and regulates DNA repair.
serine 351 phosphorylation of p62 (zeige GTF2H1 ELISA Kits) did not enhance its binding to Keap1 (zeige KEAP1 ELISA Kits) or stabilise the nuclear factor erythroid 2-related factor 2 (Nrf2 (zeige NFE2L2 ELISA Kits)) transcription factor in this neuronal context. Nrf2 (zeige NFE2L2 ELISA Kits) protein levels were markedly decreased despite transcriptional activation of the Nrf2 (zeige NFE2L2 ELISA Kits) 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 (zeige FAM126A ELISA Kits)-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