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>   首页   >   产品   >   一抗   >   精选抗体   >   SQSTM1 Antibody   

SQSTM1 Antibody

Purified Mouse Monoclonal Antibody (Mab)

     
  • 1 - SQSTM1 Antibody AM8447b
    Western blot analysis of lysate from A549 cell line, using SQSTM1 Antibody(Cat. #AM8447b). AM8447b was diluted at 1:1000. A goat anti-mouse IgG H&L(HRP) at 1:3000 dilution was used as the secondary antibody. Lysate at 20μg.
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Product info
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, E
Primary Accession Q13501
Reactivity Human
Host Mouse
Clonality Monoclonal
Isotype IgG1,κ
Clone Names 1336CT763.152.125
Calculated MW 47687 Da
Additional info
Gene ID 8878
Other Names Sequestosome-1, EBI3-associated protein of 60 kDa, EBIAP, p60, Phosphotyrosine-independent ligand for the Lck SH2 domain of 62 kDa, Ubiquitin-binding protein p62, SQSTM1, ORCA, OSIL
Target/Specificity This SQSTM1 antibody is generated from mice immunized with a recombinant protein.
Dilution WB~~1:1000
StorageMaintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
PrecautionsSQSTM1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name SQSTM1
Synonyms ORCA, OSIL
Function Autophagy receptor that interacts directly with both the cargo to become degraded and an autophagy modifier of the MAP1 LC3 family. Required both for the formation and autophagic degradation of polyubiquitin-containing bodies, called ALIS (aggresome-like induced structures) and links ALIS to the autophagic machinery. Involved in midbody ring degradation. May regulate the activation of NFKB1 by TNF-alpha, nerve growth factor (NGF) and interleukin- 1. May play a role in titin/TTN downstream signaling in muscle cells. May regulate signaling cascades through ubiquitination. Adapter that mediates the interaction between TRAF6 and CYLD (By similarity). May be involved in cell differentiation, apoptosis, immune response and regulation of K(+) channels.
Cellular Location Cytoplasm. Late endosome. Lysosome. Cytoplasmic vesicle, autophagosome. Nucleus. Endoplasmic reticulum. Cytoplasm, P-body. Note=Sarcomere (By similarity). In cardiac muscles localizes to the sarcomeric band (By similarity) Commonly found in inclusion bodies containing polyubiquitinated protein aggregates. In neurodegenerative diseases, detected in Lewy bodies in Parkinson disease, neurofibrillary tangles in Alzheimer disease, and HTT aggregates in Huntington disease. In protein aggregate diseases of the liver, found in large amounts in Mallory bodies of alcoholic and nonalcoholic steatohepatitis, hyaline bodies in hepatocellular carcinoma, and in SERPINA1 aggregates. Enriched in Rosenthal fibers of pilocytic astrocytoma In the cytoplasm, observed in both membrane-free ubiquitin- containing protein aggregates (sequestosomes) and membrane- surrounded autophagosomes. Colocalizes with TRIM13 in the perinuclear endoplasmic reticulum. Co-localizes with TRIM5 in the cytoplasmic bodies.
Tissue Location Ubiquitously expressed.
Research Areas

BACKGROUND

Required both for the formation and autophagic degradation of polyubiquitin-containing bodies, called ALIS (aggresome-like induced structures). Links ALIS to the autophagic machinery via direct interaction with MAP1 LC3 family members. May regulate the activation of NFKB1 by TNF-alpha, nerve growth factor (NGF) and interleukin-1. May play a role in titin/TTN downstream signaling in muscle cells. May regulate signaling cascades through ubiquitination. Adapter that mediates the interaction between TRAF6 and CYLD (By similarity). May be involved in cell differentiation, apoptosis, immune response and regulation of K(+) channels.

REFERENCES

Devergne O.,et al.J. Virol. 70:1143-1153(1996).
Joung I.,et al.Proc. Natl. Acad. Sci. U.S.A. 93:5991-5995(1996).
Ota T.,et al.Nat. Genet. 36:40-45(2004).
Schmutz J.,et al.Nature 431:268-274(2004).
Vadlamudi R.K.,et al.FEBS Lett. 435:138-142(1998).

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