Tyrosine kinases in inflammatory dermatologic disease

被引:7
|
作者
Paniagua, Ricardo T. [1 ,2 ]
Fiorentino, David F. [3 ]
Chung, Lorinda [1 ,2 ]
Robinson, William H. [1 ,2 ]
机构
[1] Vet Affairs Hlth Care Syst, Palo Alto Dept, Geriatr Res Educ & Clin Ctr, Palo Alto, CA 94304 USA
[2] Stanford Univ, Dept Med, Sch Med, Div Rheumatol & Immunol, Stanford, CA 94305 USA
[3] Stanford Univ, Dept Dermatol, Sch Med, Stanford, CA 94305 USA
基金
美国国家卫生研究院;
关键词
autoimmune; dermatology; dermatomyositis; fibrosis; inflammatory; pemphigus; phosphorylation; psoriasis; tyrosine kinase; GROWTH-FACTOR RECEPTOR; IMATINIB MESYLATE; PEMPHIGUS-VULGARIS; SYSTEMIC FIBROSIS; PDGF RECEPTOR; I INTERFERON; FACTOR-BETA; STIMULATORY AUTOANTIBODIES; SKIN INFLAMMATION; FACTOR-ALPHA;
D O I
10.1016/j.jaad.2010.04.026
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Tyrosine kinases (TKs) are enzymes that catalyze the phosphorylation of tyrosine residues on protein substrates. They are key components of signaling pathways that drive an array of cellular responses including proliferation, differentiation, migration, and survival. Specific TKs have recently been identified as critical to the pathogenesis of several autoimmune and inflammatory diseases. Small-molecule inhibitors of TKs are emerging as a novel class of therapy that may provide benefit in certain patient subsets. In this review, we highlight TK signaling implicated in inflammatory dermatologic diseases, evaluate strategies aimed at inhibiting these aberrant signaling pathways, and discuss prospects for future drug development. (J Am Acad Dermatol 2011;65:389-403.)
引用
收藏
页码:389 / 403
页数:15
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