anti-SQSTM1 (SQSTM1) Antikörper

Human Sequestosome 1 (SQSTM1) Interaktionspartner

1. results demonstrated that UVA up-regulates p62 and induces a p62-Nrf2 positive feedback loop to counteract oxidative stress

2. Knockdown of p62 or GABARAPL1 reduced cell survival upon proteasome inhibition.

3. Both SQSTM1-HDAC6-dependent autophagy and the aggresome pathway mediate CDK1 degradation in human breast cancer cells.

4. Authors demonstrate a novel mode of regulation of the Keap1-Nrf2 system, mediated by a splicing variant of p62/Sqstm1 pre-mRNA. Ensembl database searches and subsequent biochemical analyses of mice revealed the presence of an mRNA that encodes a p62/Sqstm1 protein lacking the Keap1-interacting region (KIR), which is essential for the interaction with Keap1.

5. High expression of LC3, beclin 1 and p62 was significantly more frequent in high-grade gliomas than in low-grade.Kaplan-Meier analyses revealed that LC3, p62 and autophagy status were significantly associated with poorer survival.

6. p62 plays an anti-apoptotic role in esophageal squamous carcinoma cells via stabilizing SKP2 under serum starvation condition.p62 affects SKP2 expression through ubiquitination.

7. Data show that p62 loss in adipocytes leads to aggressive prostate tumors by increasing osteopontin secretion, which mediates tumor fatty acid oxidation and invasion. P62 deficiency also represses energy consuming pathways in adipocytes, increasing nutrient availability for tumors.

8. P62 promotes metastasis of prostate cancer by sustaining the level of HDAC6 to inhibit autophagy and promote epithelial-to-mesenchymal transition.

9. Results provide evidence that autophagy mediates epithelial cancer chemoresistance by reducing SQSTM1 accumulation.

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

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

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

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

14. High p62 cytoplasmic expression on its own (p

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

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

17. 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.

18. 27-OH induced autophagy is dependent on the relation between nuclear factor erythroid 2 p45-related factor 2 (Nrf2)-dependent antioxidant response and p62.

19. 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

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

Mouse (Murine) Sequestosome 1 (SQSTM1) Interaktionspartner

1. Knockdown of p62 or GABARAPL1 reduced cell survival upon proteasome inhibition.

2. Authors demonstrate a novel mode of regulation of the Keap1-Nrf2 system, mediated by a splicing variant of p62/Sqstm1 pre-mRNA. Ensembl database searches and subsequent biochemical analyses of mice revealed the presence of an mRNA that encodes a p62/Sqstm1 protein lacking the Keap1-interacting region (KIR), which is essential for the interaction with Keap1.

3. the effect of the p62 P394L mutation on osteoclastogenesis and bone morphometry in relation to ageing, the natural history of lesion progression in p62(P394L) mice, is reported.

4. Drp1-dependent mitochondrial fission regulates p62-mediated autophagy in LPS-induced activated microglial cells

5. Here we show that Ulk2 heterozygous (Ulk2+/-) mice have upregulated expression of sequestosome-1/p62, an autophagy-associated stress response protein, predominantly in pyramidal neurons of the prefrontal cortex (PFC), and exhibit behavioral deficits associated with the PFC functions, including attenuated sensorimotor gating and impaired cognition

6. Autophagy through p62 plays an important role in regulating insulin receptor substrate 1 protein levels in response to nutritional deficiency. The present findings suggest that autophagy might function as energy depletion-sensing machinery that finely tunes insulin signal transduction.

7. 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.

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

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

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

11. 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.

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

13. 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.

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

15. 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.

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

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

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

19. 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.

20. 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

Zebrafish Sequestosome 1 (SQSTM1) Interaktionspartner

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.