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anti-Human SQSTM1 Antikörper:
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Human Monoclonal SQSTM1 Primary Antibody für IF, ELISA - ABIN563860
Jung, Chung, Won Kim, Kim, Komatsu, Tanaka, Nguyen, Kang, Yoon, Kim, Jeong, Han, Lee, Kim, Shin, Lee: Loss of autophagy diminishes pancreatic beta cell mass and function with resultant hyperglycemia. in Cell metabolism 2008
Show all 88 Pubmed References
Human Polyclonal SQSTM1 Primary Antibody für ICC, IF - ABIN4343147
Pyo, Yoo, Ahn, Nah, Hong, Kam, Jung, Jung: Overexpression of Atg5 in mice activates autophagy and extends lifespan. in Nature communications 2013
Show all 51 Pubmed References
Human Polyclonal SQSTM1 Primary Antibody für ICC, IF - ABIN4343150
Gispert, Brehm, Weil, Seidel, Rüb, Kern, Walter, Roeper, Auburger: Potentiation of neurotoxicity in double-mutant mice with Pink1 ablation and A53T-SNCA overexpression. in Human molecular genetics 2015
Show all 7 Pubmed References
Human Polyclonal SQSTM1 Primary Antibody für ELISA, ICC - ABIN6263985
Wu, Huang, Jiao, Ding, Zhang, Chen, Wang, Li, Huo: Olaquindox disrupts tight junction integrity and cytoskeleton architecture in mouse Sertoli cells. in Oncotarget 2017
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Human Polyclonal SQSTM1 Primary Antibody für IHC (fro), IHC (p) - ABIN3043937
Li, Jen, Wu, Lee, Fang, Quigley, Lee, Wang, Zhou, Vergnes, Chen, Li, Reue, Ann, Hsiai: Disturbed Flow Induces Autophagy, but Impairs Autophagic Flux to Perturb Mitochondrial Homeostasis. in Antioxidants & redox signaling 2016
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Human Polyclonal SQSTM1 Primary Antibody für IF (p), IHC (p) - ABIN682153
Cui, Luo, Li, Li, Wang: Changes of intracellular Ca2+ in quercetin-induced autophagy progression. in Acta biochimica et biophysica Sinica 2015
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Human Monoclonal SQSTM1 Primary Antibody für ELISA, WB - ABIN522359
Kirkin, Lamark, Sou, Bjørkøy, Nunn, Bruun, Shvets, McEwan, Clausen, Wild, Bilusic, Theurillat, Øvervatn, Ishii, Elazar, Komatsu, Dikic, Johansen: A role for NBR1 in autophagosomal degradation of ubiquitinated substrates. in Molecular cell 2009
Show all 4 Pubmed References
Human Polyclonal SQSTM1 Primary Antibody für ICC, IF - ABIN449246
Zhang, Gui, Huang, Deng, Fang, Ke, He, Li, Fang: Neuroprotective Effects of β-Asarone Against 6-Hydroxy Dopamine-Induced Parkinsonism via JNK/Bcl-2/Beclin-1 Pathway. in Molecular neurobiology 2016
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Human Polyclonal SQSTM1 Primary Antibody für ICC, IHC (p) - ABIN3044026
Jeong, He, Nohara, Park, Shin, Kim, Shimomura, Koike, Yoo, Chen: Dual attenuation of proteasomal and autophagic BMAL1 degradation in Clock Δ19/+ mice contributes to improved glucose homeostasis. in Scientific reports 2017
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Human Polyclonal SQSTM1 Primary Antibody für IF, IHC (p) - ABIN542770
Ju, Miller, Hanson, Weihl: Impaired protein aggregate handling and clearance underlie the pathogenesis of p97/VCP-associated disease. in The Journal of biological chemistry 2008
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These findings on the role of p62(TRM) provide new insights into SQSTM1-linked diseases and mTORC1 signaling.
Data indicated that p62 colocalized and associated with the different ASP clade representatives and that this association led to induction of autophagy. Despite the implication of the homodimerization domain of p62 in its association with ASP, ASP is ubiquitinated, which impacts its abundance in its monomeric and multimeric forms.
p38delta promotes micro-aggregate transport by phosphorylating SQSTM1, a major scaffold protein that assembles soluble ubiquitylated proteins into micro-aggregates.
Results show that, in order to specifically associate with activated LC3 exported from the nucleus, p62 must use a mechanism to discriminate non-activated LC3 in the cytoplasm and that p62 only binds to deacetylated LC3.
Results show that p62 binds to IGF2BP1 to control the mRNA stability of FERMT2 and multiple pro-metastatic factors. This p62-RBP interaction distinguishes melanoma from other tumors where p62 controls autophagy or oxidative stress.
the recruitment of the FIP200 CTR slows the phase separation of ubiquitinated proteins by p62 in a reconstituted system. Our data provide the molecular basis for a crosstalk between cargo condensation and autophagosome formation.
TRIM16 acts as a scaffold protein and, by interacting with p62, ULK1, ATG16L1, and LC3B, facilitates autophagic degradation of protein aggregates.
P62 regulate selective autophagy, cell survival, cell death, oxidative stress, DNA repair and inflammation, and to play a role in a number of diseases. [review]
Flightless-I functions as a checkpoint protein for selective autophagy by interacting with p62 to block its recognition of LC3, leading to tumorigenesis in breast cancer.
Recombinant p62 does not undergo phase separation in vitro; however, adding a K63 polyubiquitin chain to p62 induces p62 phase separation, which results in enrichment of high-molecular weight ubiquitin signals in p62 droplets. Mixing recombinant p62 with cytosol from p62(-/-) cells also results in p62 phase separation in a polyubiquitination-dependent manner.
Increased SQSTM1 expression is associated with myeloid leukemia progression.
A neurodegenerative disorder affecting 3 Iranian families is caused by biallelic inactivating mutations in SQSTM1.
PHB2 forms a ternary protein complex with sequestosome 1 (SQSTM1) and LC3, leading to loading of LC3 onto the damaged mitochondria.
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
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.
identification of a TIA1 variant that drives myodegeneration in multisystem proteinopathy with SQSTM1 mutations
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.
The KEAP1 R320Q and R470C ANCHOR mutants colocalize with NRF2, p62/SQSTM1, and polyubiquitin.
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.
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.
SQSTM1 is essential for the anti-inflammatory capacity of CpdA, at least in macrophage cells.
In mice lacking both Drp1 and p62, the additional loss of p62 significantly extended the survival of Purkinje neurons lacking Drp1.
Findings suggest that p62 is crucial for cytoprotection against MeHg-induced toxicity and is required for MeHg-induced ubiquitinated protein clearance.
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.
Letter: Suppression of autophagy perturbs turnover of sequestosome-1/p62 in Merkel cells but not in keratinocytes.
Knockdown of p62 or GABARAPL1 reduced cell survival upon proteasome inhibition.
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.
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.
Drp1-dependent mitochondrial fission regulates p62-mediated autophagy in LPS-induced activated microglial cells
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
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.
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.
the essential role that p62, particularly its PB1 and UBA domains, has in the formation of ALIS.
Cereblon suppresses the formation of pathogenic protein aggregates in a p62-dependent manner.
A complex of C9ORF72 and p62 uses arginine methylation to eliminate stress granules by autophagy.
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.
These results suggest that overexpression of SQSTM1 in SOD1 (H46R) mice accelerates disease onset by compromising the protein degradation pathways.
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.
The studies findings imply that p62 signaling plays a crucial role in suppressing inflammatory cytokine production by globular adiponectin in macrophages.
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