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Silence of p62 promotes apoptosis induced by mitochondrial depolarization.
Rare variants in SQSTM1 are risk for sporadic inclusion body myositis.
The WDR81 (show WDR81 ELISA Kits) coordinates p62 (show GTF2H1 ELISA Kits) and LC3C to facilitate autophagic removal of Ub proteins, and provide important insights into CAMRQ2 (show WDR81 ELISA Kits) syndrome, a WDR81 (show WDR81 ELISA Kits)-related developmental disorder.
SQSTM1-Nup214 (show NUP214 ELISA Kits), although mostly cytoplasmic, also forms nuclear bodies and inhibits nuclear protein (show RDBP ELISA Kits) but not poly(A)(+) RNA export.
autophagy upregulation by Sequestosome 1 (p62/SQSM1) knockdown ameliorated this cell injury and relieved insulin (show INS ELISA Kits) resistance
This work suggests that UVA-induced p62 (show GTF2H1 ELISA Kits) acts through COX-2 (show COX2 ELISA Kits) to promote skin tumor growth and progression.
we provide evidence that p62 (show GTF2H1 ELISA Kits) is implicated in the activation of NF-kappaB (show NFKB1 ELISA Kits) signaling that is partly dependent on RIP1
In this study, we first observed that p62-positive intranuclear aggregates also appeared in controls and were not specific for the Neuronal Intranuclear Hyaline Inclusion Disease cases.
Data suggest that phosphorylation of SQSTM1 by AMP-activated protein kinase (AMPK (show PRKAA2 ELISA Kits)) and translocation of SQSTM1 to mitochondria drives autophagic cell death in adult hippocampal neural stem cells; activation of AMPK (show PRKAA1 ELISA Kits) promotes autophagic cell death; inhibition of AMPK (show PRKAA1 ELISA Kits) (by enzyme inhibitor or RNA interference) suppresses autophagic cell death. (SQSTM1 = sequestosome 1)
Authors found that p62/SQSTM1, a protein upregulated in liver parenchymal cells but downregulated in HCC (show FAM126A ELISA Kits)-associated HSCs, negatively controls hepatic stellate cells activation.
serine 351 phosphorylation of p62 (show GTF2H1 ELISA Kits) did not enhance its binding to Keap1 (show KEAP1 ELISA Kits) or stabilise the nuclear factor erythroid 2-related factor 2 (Nrf2 (show NFE2L2 ELISA Kits)) transcription factor in this neuronal context. Nrf2 (show NFE2L2 ELISA Kits) protein levels were markedly decreased despite transcriptional activation of the Nrf2 (show 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.
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.
role of p62 (show GTF2H1 ELISA Kits) in MDB (show ABR ELISA Kits) maturation and stability
two ALS-linked factors, SQSTM1 and ALS2 (show ALS2 ELISA Kits), have distinct but additive protective roles against mutant SOD1 (show SOD1 ELISA Kits)-mediated toxicity by modulating neuronal proteostasis possibly through the autophagy-endolysosomal system.
These results demonstrated that p62-dependent mitophagy has an immunosuppressive role to innate immune response and might serve as a potential immunomodulatory target for inflammation-associated diseases.
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