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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.
The model reveals a compensatory autophagic pathway, mediated by a SQSTM1/p62-dependent clearance of accumulated polyubiquitinated proteins. In addition to mediating the sequestration of ubiquitinated cargos into phagophores, the precursors to autophagosomes, SQSTM1 is also important for polyubiquitinated aggregate formation upon proteasomal inhibition.
ESI (show PI3 Proteins) induces protective autophagy of lung cancer cells through Nrf2 (show GABPA Proteins)-p62 (show GTF2H1 Proteins)-keap1 (show KEAP1 Proteins) feedback loop
IFN-gamma induces activated but insufficient autophagy and thus contributes to a degree to p62-dependent apoptosis of nasal epithelial cells in chronic rhinosinusitis with nasal polyps.
The underling mechanism of autophagy/p62 (show GTF2H1 Proteins)/Nrf2 (show GABPA Proteins) pathway discovered may provide a new direction for drug development.
Study show the proteasome autophagy mechanism is mediated by the p62/SQSTM1 adapter and requires its ubiquitin-associated domain. Independently, p62 (show GTF2H1 Proteins) serves also as a shuttling protein for ubiquitinated substrates, using its PB1 (show SMR3A Proteins) domain. This places p62 (show GTF2H1 Proteins) in a pivotal position where under certain conditions it binds to the proteasome as a protease, whereas in other conditions it recognizes the proteasome as a prey.
The study describes a previously uncharacterized cellular response induced by heme: the formation of p62/SQSTM1 aggregates containing ubiquitinated proteins in structures known as aggresome-like induced structures (ALIS). This action is part of a response driven by the transcription factor NRF2 (show GABPA Proteins) to the excessive generation of reactive oxygen species induced by heme.
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.
this study proved that SYVN1 (show SYVN1 Proteins) enhances SERPINA1 (show SERPINA1 Proteins)(E342K)/ATZ degradation through SQSTM1-dependent autophagy and attenuates SERPINA1 (show SERPINA1 Proteins)(E342K)/ATZ cytotoxicity.
Data suggest that maternal nutrition modulates expression of autophagy proteins p62/Sqstm1 and Lc3 (show MAP1LC3A Proteins)-II/Map1lc3 (show MAP1LC3B Proteins) in liver and hypothalamus of offspring (newborn, suckling, and adult stages); for example, high-fat diet leading to maternal obesity up-regulates p62 (show GTF2H1 Proteins) and down-regulates Lc3 (show MAP1LC3A Proteins)-II in neonatal liver. (p62/Sqstm1 = sequestosome 1; Lc3 (show MAP1LC3A Proteins)-II/Map1lc3 (show MAP1LC3B Proteins) = microtubule-associated protein (show SPAG5 Proteins) 1-light chain 3)
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