3,4,5-三甲氧基肉桂酸 90-50-6价格

rcells. This PTP has been shown to be an essential regulator of T- and B-cell antigen receptor signaling. It functions through either direct interaction with components of the antigen receptor complexes, or by activating various Src family kinases required for the antigen receptor signaling. This PTP also suppresses JAK kinases, and thus functions as a regulator of cytokine receptor signaling. Four alternatively spliced transcripts variants of this gene, which encode distinct isoforms, have been reported. [provided by RefSeq, Jul 2008].

Function : Protein tyrosine-protein phosphatase required for T-cell activation through the antigen receptor. Acts as a positive regulator of T-cell coactivation upon binding to DPP4. The first PTPase domain has enzymatic activity, while the second one seems to affect the substrate specificity of the first one. Upon T-cell activation, recruits and dephosphorylates SKAP1 and FYN. Dephosphorylates LYN, and thereby modulates LYN activity.

Subunit : Binds GANAB and PRKCSH. Interacts with SKAP1. Interacts with DPP4; the interaction is enhanced in a interleukin-12-dependent manner in activated lymphocytes. Contains 2 tyrosine-protein phosphatase domains.

Subcellular Location : Membrane; Single-pass type I membrane protein. Membrane raft. Note=Colocalized with DPP4 in membrane rafts.

Post-translational modifications : Heavily N- and O-glycosylated.

3,4,5-三甲氧基肉桂酸 90-50-6价格DISEASE : Defects in PTPRC are a cause of severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell-positive/NK-cell-positive (T(-)B(+)NK(+) SCID) [MIM:608971]. A form of severe combined immunodeficiency (SCID), a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients present in infancy recurrent,