Reactive species
Human;Rat;Mouse;
Antibody type
Polyclonal Antibody
Gene Name
ITGA2B GP2B ITGAB
Protein name
ITGA2B (heavy chain, Cleaved-Leu32)
Immunogen
Synthesized peptide derived from human ITGA2B (heavy chain, Cleaved-Leu32)
Specificity
This antibody detects endogenous levels of Human ITGA2B (heavy chain, Cleaved-Leu32, protein was cleaved amino acid sequence between 31-32 )
Constitute
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Source
Polyclonal, Rabbit,IgG
Dilution rate
WB 1:500-2000;IHC-p 1:50-300
Purification process
The antibody was affinity-purified from rabbit serum by affinity-chromatography using specific immunogen.
Other name
Integrin alpha-IIb (GPalpha IIb;GPIIb;Platelet membrane glycoprotein IIb;CD antigen CD41) [Cleaved into: Integrin alpha-IIb heavy chain; Integrin alpha-IIb light chain, form 1; Integrin alpha-IIb light chain, form 2]
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
