Product Pathways - Lymphocyte Signaling
PTPN22 Antibody #12447
Reactivity Key: H=Human
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Specificity / Sensitivity
PTPN22 Antibody recognizes endogenous levels of total PTPN22 protein.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding His301 of human PTPN22 protein. Antibodies are purified by protein A and peptide affinity chromatography.
Western blot analysis of extracts from Daudi and NK-92 cells using PTPN22 Antibody.
Western blot analysis of extracts from 293T cells, mock transfected (-) or transfected with a construct expressing Myc/DDK-tagged full-length human PTPN22 (hPTPN22-Myc/DDK; +), using PTPN22 Antibody.
Immunoprecipitation of PTPN22 from Daudi cell extracts, using Normal Rabbit IgG #2729 (lane 2) or PTPN22 Antibody (lane 3). Lane 1 is 10% input. Western blot analysis was performed using PTPN22 Antibody.
PTPN22 (Lyp/PEP) is a cytoplasmic phosphatase expressed by hematopoietic cells (1,2). PTPN22 associates with the tyrosine kinase Csk to inhibit T cell receptor signaling through inactivation of Src kinases (3,4). Csk phosphorylates Src kinases on an inhibitory tyrosine, while PTPN22 dephosphorylates an activating site (4). PTPN22(-/-) mice have higher levels of activated Lck than wild-type, resulting in greater T cell expansion and increased serum antibody levels (5). Research studies have shown that a single-nucleotide polymorphism, 1858T of the PTPN22 gene which encodes the amino acid substitution R620W, confers increased risk for multiple autoimmune diseases including type I diabetes, rheumatoid arthritis, systemic lupus erythematosus, and Graves disease (6-9). Interestingly, although the R620W substitution disrupts the interaction between Csk and PTPN22, it is actually a gain-of-function mutation resulting in increased phosphatase activity (6,10,11). Recent evidence suggests that the autoimmune phenotype associated with the R620W variant is the result of increased calpain-mediated degradation and decreased protein levels of PTPN22 (12).
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- Kyogoku, C. et al. (2004) Am J Hum Genet 75, 504-7.
- Velaga, M.R. et al. (2004) J Clin Endocrinol Metab 89, 5862-5.
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For Research Use Only. Not For Use In Diagnostic Procedures.