Target：CD41
Fields：Rap1 signaling pathway;PI3K-Akt signaling pathway;Focal adhesion;ECM-receptor interaction;Platelet activation;Neutrophil extracellular trap formation;Hematopoietic cell lineage;Regulation of actin cytoskeleton;Human papillomavirus infection;Pathways in cancer;Small cell lung cancer;Hypertrophic cardiomyopathy;Arrhythmogenic right ventricular cardiomyopathy;Dilated cardiomyopathy;Fluid shear stress and atherosclerosis
Gene Name：ITGA2B
Protein Name：Integrin alpha-IIb
Human Gene Id：3674
Human Swiss Prot No：P08514
Mouse Gene Id：16399
Mouse Swiss Prot No：Q9QUM0
Immunogen：Synthetic Peptide of CD41
Specificity：The antibody detects endogenous human CD41/ Intergrin α2b protein.
Formulation：PBS, pH 7.4, containing 0.5%BSA, 0.02% sodium azide as Preservative and 50% Glycerol.
Source：Monoclonal, Mouse
Dilution：IHC 1:100. IF 1:50-200
Purification：The antibody was affinity-purified from mouse ascites by affinity-chromatography using specific immunogen.
Storage Stability：-15°C to -25°C/1 year(Do not lower than -25°C)
Other Name：ITGA2B;GP2B;ITGAB;Integrin alpha-IIb;GPalpha IIb;GPIIb;Platelet membrane glycoprotein IIb;CD41
Molecular Weight(Da)：113kD
Background： This gene encodes a member of the integrin alpha chain family of proteins. The encoded preproprotein is proteolytically processed to generate light and heavy chains that associate through disulfide linkages to form a subunit of the alpha-IIb/beta-3 integrin cell adhesion receptor. This receptor plays a crucial role in the blood coagulation system, by mediating platelet aggregation. Mutations in this gene are associated with platelet-type bleeding disorders, which are characterized by a failure of platelet aggregation, including Glanzmann thrombasthenia. [provided by RefSeq, Jan 2016],
Function：disease:Defects in ITGA2B are a cause of Glanzmann thrombasthenia (GT) [MIM:273800]; also known as thrombasthenia of Glanzmann and Naegeli. This autosomal recessive disorder is the most common inherited disease of platelets. GT is characterized by mucocutaneous bleeding of mild-to-moderate severity and the inability of this integrin to recognize macromolecular or synthetic peptide ligands. GT has been classified clinically into types I and II. In type I, platelets show absence of the glycoprotein IIb/beta-3 complexes at their surface and lack fibrinogen and clot retraction capability. In type II, the platelets express the glycoprotein IIb/beta-3 complex at reduced levels (5-20% controls), have detectable amounts of fibrinogen, and have low or moderate clot retraction capability. The platelets of GT 'variants' have normal or near normal (60-100%) expression of dysfunctional receptors.,fun
Subcellular Location：Membrane; Single-pass type I membrane protein.
Expression：Isoform 1 and isoform 2 are expressed in platelets and megakaryocytes, but not in reticulocytes. Not detected in Jurkat, nor in U937 cell lines (PubMed:2351656). Isoform 3 is expressed in prostate adenocarcinoma, as well as in several erythroleukemia, prostate adenocarcinoma and melanoma cell lines, including PC-3, DU-145, HEL, WM983A, WM983B and WM35. Not detected in platelets, nor in normal prostate (at protein level) (PubMed:9809974).
