Browse our anti-SQSTM1 (SQSTM1) Antibodies

Human Sequestosome 1 (SQSTM1) interaction partners

1. Cereblon suppresses the formation of pathogenic protein aggregates in a p62-dependent manner.

2. Study shows that p62 hijacked NOXA for its degradation during autophagy.

3. A complex of C9ORF72 and p62 uses arginine methylation to eliminate stress granules by autophagy.

4. Study demonstrated that the expression of p62 was upregulated in 4nitroquinoline1oxideinduced oral carcinogenesis, accompanied with myeloidderived suppressor cells and regulatory T cells accumulation.

5. High p62 cytoplasmic expression on its own (p

6. the complex structures between the ZZ-domain of p62 and various type-1 and type-2 N-degrons, are reported.

7. the role of p62 in energy metabolism was studied in fibroblasts.

8. p62 and ubiquitinated proteins spontaneously coalesce into larger clusters. Efficient cluster formation requires substrates modified with at least two ubiquitin chains longer than three moieties and is based on p62 filaments cross-linked by the substrates.

9. 27-OH induced autophagy is dependent on the relation between nuclear factor erythroid 2 p45-related factor 2 (Nrf2)-dependent antioxidant response and p62.

10. our results showed that high CD44 led to p62-associated NRF2 activation in CD44(high) breast CSC-like cells. NRF2 activation contributed to the aggressive phenotype, tumor growth, and anticancer drug resistance of CD44(high) CSCs

11. results suggested that p62 plays a protective role in adipogenesis of human adipose-derived stromal cells through regulating mitophagy.

12. 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.

13. 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.

14. 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.

15. 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.

16. p62 deficiency in stromal fibroblasts promotes resistance to glutamine deprivation by the direct control of ATF4 stability through its p62-mediated polyubiquitination.

17. 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

18. The results suggest that p62 may be an effective predictor of prognosis and a potential target for therapy in osteosarcoma.

19. 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.

20. ESI induces protective autophagy of lung cancer cells through Nrf2-p62-keap1 feedback loop

Mouse (Murine) Sequestosome 1 (SQSTM1) interaction partners

1. These results indicate that p62 predominantly suppresses murine in vitro osteoclast differentiation and highlight previously undetected Paget's disease-like phenotypes in p62(-/-) mice in vivo.

2. the essential role that p62, particularly its PB1 and UBA domains, has in the formation of ALIS.

3. Cereblon suppresses the formation of pathogenic protein aggregates in a p62-dependent manner.

4. A complex of C9ORF72 and p62 uses arginine methylation to eliminate stress granules by autophagy.

5. Atg7(f/f) Tyr-Cre mice, in which autophagy-related 7 (Atg7) is conditionally deleted under the control of the tyrosinase promoter, are a model for accumulations of the autophagy adapter and substrate sequestosome-1/p62 in both neuronal and neuroepithelial cells.

6. These results suggest that overexpression of SQSTM1 in SOD1 (H46R) mice accelerates disease onset by compromising the protein degradation pathways.

7. these results suggested that trehalose can function as a novel activator of the p62-Keap1/Nrf2 pathway, in addition to inducing autophagy. Therefore, trehalose may be useful to treat many chronic diseases involving oxidative stress and dysfunction of autophagy.

8. The studies findings imply that p62 signaling plays a crucial role in suppressing inflammatory cytokine production by globular adiponectin in macrophages.

9. 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.

10. Deletion of both p62/Sqstm1 and Nrf2 genes spontaneously leads to the development of NASH.

11. p62 serves to prevent endoplasmic reticulum stress in mouse hypothalamus by maintaining protein folding capacity

12. The p62-keap1-Nrf2 antioxidant pathway was primarily activated in the early stage of APAP hepatotoxicity.

13. 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.

14. analysis of soluble SQSTM1 complexes and soluble complexes formed between SQSTM1 oligomers and LC3 using a combination of fluorescence microscopy-based biophysical approaches in living cells

15. ENC1 interacts with the phosphorylated p62 to impair autophagic degradation of mutant huntingtin protein aggregates.

16. this study proved that SYVN1 enhances SERPINA1(E342K)/ATZ degradation through SQSTM1-dependent autophagy and attenuates SERPINA1(E342K)/ATZ cytotoxicity.

17. Data suggest that maternal nutrition modulates expression of autophagy proteins p62/Sqstm1 and Lc3-II/Map1lc3 in liver and hypothalamus of offspring (newborn, suckling, and adult stages); for example, high-fat diet leading to maternal obesity up-regulates p62 and down-regulates Lc3-II in neonatal liver. (p62/Sqstm1 = sequestosome 1; Lc3-II/Map1lc3 = microtubule-associated protein 1-light chain 3)

18. TRIM11 suppresses AIM2 inflammasome by degrading AIM2 via p62-dependent selective autophagy.

19. SQSTM1 dynamically associates with DNA damage foci (DDF) and regulates DNA repair.

20. Thyroid hormone promotes selective autophagy via induction of DAPK2-SQSTM1 cascade, which in turn protects hepatocytes from diethylnitrosamine-induced hepatotoxicity or carcinogenesis.

Zebrafish Sequestosome 1 (SQSTM1) interaction partners

1. 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.