CD61

CD61NCBI

CD61

PHA stimulated peripheral blood cells.

This product requires protein digestion pre-treatment of paraffin sections e. g. trypsin prior to staining.

Phosphate buffered saline pH7. 4

Use 10ul of the suggested working dilution to label 1x106 cells in 100ul. Suggested

Integrin alpha-V/beta-3 is a receptor for cytotactin fibronectin laminin matrix metalloproteinase-2 osteopontin osteomodulin prothrombin thrombospondin vitronectin and von Willebrand factor. Integrin alpha-IIb/beta-3 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. In case of HIV-1 infection the interaction with extracellular viral Tat protein seems to enhance angiogenesis in Kaposi\' s sarcoma lesions.

Membrane; Single-pass type I membrane protein.

Phosphorylated on tyrosine residues in response to thrombin-induced platelet aggregation. Probably involved in outside-in signaling. A peptide (AA 740-762) is capable of binding GRB2 only when both Tyr-773 and Tyr-785 are phosphorylated. SHC binding also occurs when Tyr-785 alone is phosphorylated.

Position 169 is associated with platelet-specific alloantigen HPA-4 (PEN or YUK). HPA-4A/PEN(A)/YUK(A) has Arg-169 and HPA-4B/PEN(B)/YUK(B) has Gln-169. HPA-4B is involved in neonatal alloimmune thrombocytopenia (NAIT or NATP).

Position 515 is associated with platelet-specific alloantigen CA/TU. CA(-)/TU(-) has Arg-515 and CA(+)/TU(+) has Gln-515. CA(+) is involved in NAIT.

Defects in ITGB3 are a cause of Glanzmann thrombasthenia (GT) [MIM:273800]; also known as thrombasthenia of Glanzmann and Naegeli. GT is the most common inherited disease of platelets. Its inheritance is autosomal recessive. It 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-IIIa complexes at their surface and lack fibrinogen and clot retraction capability. In type II the platelets express the GPIIb-IIIa 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.

Contains 1 VWFA domain. 1. Phillips. D. R. et al. (1991) GPIIb-IIIa: the responsive integrin. 2. Hynes. R. O. (1992) Integrins: versatility. modulation. and signaling in cell adhesion. 3. Michelson. A. D. et al. (1995) A panel of platelet mAb for the study of haemostasis and thrombosis in baboons. Leucocyte Typing V. Oxford University Press p 1230-1231. 4. Gatter. K. et al. (1998) The immunohistological detection of platelets. megakaryocytes and thrombi in routinely processed specimens.