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CD61 Antibody

Purified Rabbit Polyclonal Antibody (Pab)

     
  • 1 - CD61 Antibody AP53351
    Anti-CD61 Antibody at 1:1000 dilution + U-87 MG whole cell lysate Lysates/proteins at 20 µg per lane. Secondary Goat Anti-Rabbit IgG, (H+L),Peroxidase conjugated at 1/10000 dilution. Predicted band size : 87 kDa Blocking/Dilution buffer: 5% NFDM/TBST.
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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
Primary Accession P05106
Reactivity Human
Host Rabbit
Clonality Polyclonal
Calculated MW 87 KDa
Additional info
Gene ID 3690
Other Names Integrin beta-3, Platelet membrane glycoprotein IIIa, GPIIIa, CD61, ITGB3, GP3A
Dilution WB~~ 1:1000
Format Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol
StorageStore at -20 °C.Stable for 12 months from date of receipt
Protein Information
Name ITGB3
Synonyms GP3A
Function Integrin alpha-V/beta-3 (ITGAV:ITGB3) is a receptor for cytotactin, fibronectin, laminin, matrix metalloproteinase-2, osteopontin, osteomodulin, prothrombin, thrombospondin, vitronectin and von Willebrand factor. Integrin alpha-IIb/beta-3 (ITGA2B:ITGB3) is a receptor for fibronectin, fibrinogen, plasminogen, prothrombin, thrombospondin and vitronectin. Integrins alpha-IIb/beta-3 and alpha-V/beta-3 recognize the sequence R-G-D in a wide array of ligands. Integrin alpha- IIb/beta-3 recognizes the sequence H-H-L-G-G-G-A-K-Q-A-G-D-V in fibrinogen gamma chain. Following activation integrin alpha- IIb/beta-3 brings about platelet/platelet interaction through binding of soluble fibrinogen. This step leads to rapid platelet aggregation which physically plugs ruptured endothelial surface. Fibrinogen binding enhances SELP expression in activated platelets (By similarity). ITGAV:ITGB3 binds to fractalkine (CX3CL1) and acts as its coreceptor in CX3CR1-dependent fractalkine signaling (PubMed:23125415, PubMed:24789099). ITGAV:ITGB3 binds to NRG1 (via EGF domain) and this binding is essential for NRG1-ERBB signaling (PubMed:20682778). ITGAV:ITGB3 binds to FGF1 and this binding is essential for FGF1 signaling (PubMed:18441324). ITGAV:ITGB3 binds to FGF2 and this binding is essential for FGF2 signaling (PubMed:28302677). ITGAV:ITGB3 binds to IGF1 and this binding is essential for IGF1 signaling (PubMed:19578119). ITGAV:ITGB3 binds to IGF2 and this binding is essential for IGF2 signaling (PubMed:28873464). ITGAV:ITGB3 binds to IL1B and this binding is essential for IL1B signaling (PubMed:29030430). ITGAV:ITGB3 binds to PLA2G2A via a site (site 2) which is distinct from the classical ligand-binding site (site 1) and this induces integrin conformational changes and enhanced ligand binding to site 1 (PubMed:18635536, PubMed:25398877). ITGAV:ITGB3 acts as a receptor for fibrillin-1 (FBN1) and mediates R-G-D-dependent cell adhesion to FBN1 (PubMed:12807887).
Cellular Location Cell membrane; Single- pass type I membrane protein. Cell projection, lamellipodium membrane Cell junction, focal adhesion
Tissue Location Isoform beta-3A and isoform beta-3C are widely expressed. Isoform beta-3A is specifically expressed in osteoblast cells; isoform beta-3C is specifically expressed in prostate and testis
Research Areas

BACKGROUND

Integrin alpha-V/beta-3 (ITGAV:ITGB3) is a receptor for cytotactin, fibronectin, laminin, matrix metalloproteinase-2, osteopontin, osteomodulin, prothrombin, thrombospondin, vitronectin and von Willebrand factor. Integrin alpha-IIb/beta-3 (ITGA2B:ITGB3) is a receptor for fibronectin, fibrinogen, plasminogen, prothrombin, thrombospondin and vitronectin. Integrins alpha-IIb/beta-3 and alpha-V/beta-3 recognize the sequence R-G-D in a wide array of ligands. Integrin alpha- IIb/beta-3 recognizes the sequence H-H-L-G-G-G-A-K-Q-A-G-D-V in fibrinogen gamma chain. Following activation integrin alpha- IIb/beta-3 brings about platelet/platelet interaction through binding of soluble fibrinogen. This step leads to rapid platelet aggregation which physically plugs ruptured endothelial surface. Fibrinogen binding enhances SELP expression in activated platelets (By similarity). In case of HIV-1 infection, the interaction with extracellular viral Tat protein seems to enhance angiogenesis in Kaposi's sarcoma lesions.

REFERENCES

Fitzgerald L.A.,et al.J. Biol. Chem. 262:3936-3939(1987).
Zimrin A.B.,et al.J. Clin. Invest. 81:1470-1475(1988).
Frachet P.,et al.Mol. Biol. Rep. 14:27-33(1990).
Kumar C.S.,et al.J. Biol. Chem. 272:16390-16397(1997).
Mural R.J.,et al.Submitted (SEP-2005) to the EMBL/GenBank/DDBJ databases.

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