| Literature DB >> 21190368 |
Torkel Vang1, Yuli Xie, Wallace H Liu, Dusica Vidović, Yidong Liu, Shuangding Wu, Deborah H Smith, Alison Rinderspacher, Caty Chung, Gangli Gong, Tomas Mustelin, Donald W Landry, Robert C Rickert, Stephan C Schürer, Shi-Xian Deng, Lutz Tautz.
Abstract
The lymphoid tyrosine phosphatase (Lyp, PTPN22) is a critical negative regulator of T cell antigen receptor (TCR) signaling. A single-nucleotide polymorphism (SNP) in the ptpn22 gene correlates with the incidence of various autoimmune diseases, including type 1 diabetes, rheumatoid arthritis, and systemic lupus erythematosus. Since the disease-associated allele is a more potent inhibitor of TCR signaling, specific Lyp inhibitors may become valuable in treating autoimmunity. Using a structure-based approach, we synthesized a library of 34 compounds that inhibited Lyp with IC(50) values between 0.27 and 6.2 μM. A reporter assay was employed to screen for compounds that enhanced TCR signaling in cells, and several inhibitors displayed a dose-dependent, activating effect. Subsequent probing for Lyp's direct physiological targets by immunoblot analysis confirmed the ability of the compounds to inhibit Lyp in T cells. Selectivity profiling against closely related tyrosine phosphatases and in silico docking studies with the crystal structure of Lyp yielded valuable information for the design of Lyp-specific compounds.Entities:
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Year: 2010 PMID: 21190368 PMCID: PMC3025750 DOI: 10.1021/jm101004d
Source DB: PubMed Journal: J Med Chem ISSN: 0022-2623 Impact factor: 7.446