Browse our anti-SQSTM1 (SQSTM1) Antibodies

Human Sequestosome 1 (SQSTM1) interaction partners

1. PHB2 forms a ternary protein complex with sequestosome 1 (SQSTM1) and LC3, leading to loading of LC3 onto the damaged mitochondria.

2. our results suggest that autophagy tightly controls nuclear NOTCH1 activity through multiple p62 binding sites, and that modulating autophagy activity may be useful for treating NOTCH1 related human diseases

3. The proposed prognostic model based on SQSTM1 status and N-stage can serve as a useful tool to predict the risk of distant metastasis of NPC.

4. identification of a TIA1 variant that drives myodegeneration in multisystem proteinopathy with SQSTM1 mutations

5. Here, the method to overexpress and purify p62 full-length as well as a number of p62 truncations is described, along with the protocol to assemble p62 filaments and preparation of negative stain EM grids to visualize the filaments by transmission EM. In vitro prepared p62 filaments serve as model systems to reconstitute aspects of the selective autophagy and signaling machinery.

6. The KEAP1 R320Q and R470C ANCHOR mutants colocalize with NRF2, p62/SQSTM1, and polyubiquitin.

7. p62 was significantly upregulated in colorectal cancer (CRC), and a high p62 level was an independent risk factor for a poor prognosis in CRC patients. p62 promoted CRC migration and invasion by inhibiting apoptosis and promoting cell proliferation in vitro, and p62 aggravated tumour growth and metastasis in vivo.

8. This study uncovers that the R-BiP/Beclin-1/p62 complex has an important role in the crosstalk between apoptosis and autophagy. The results also propose how mono-drug resistance can be overcome using potent combinations to improve anticancer therapy.

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

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

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

12. 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.

13. 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.

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

15. 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.

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

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

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

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

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

Mouse (Murine) Sequestosome 1 (SQSTM1) interaction partners

1. Findings suggest that p62 is crucial for cytoprotection against MeHg-induced toxicity and is required for MeHg-induced ubiquitinated protein clearance.

2. Study of ethanol-induced lipophagy in an immortalized mouse hepatocyte line, AML12 data support a model in which autophagosomes were directed to the lipid droplets (LDs) via SQSTM1, which bound to ubiquitinated proteins, possibly including perilipin 1, on LDs and provides a potential mechanistic explanation to how ethanol induces lipophagy in hepatocytes.

3. Letter: Suppression of autophagy perturbs turnover of sequestosome-1/p62 in Merkel cells but not in keratinocytes.

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

5. 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.

6. 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.

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

8. 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

9. 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.

10. 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.

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

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

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

14. 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.

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

16. 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.

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

18. 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.

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

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

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.