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Chinese Medical Journal ; (24): 3898-3904, 2012.
Artigo em Inglês | WPRIM | ID: wpr-256621

RESUMO

Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a member of the TNF superfamily of structurally related cytokines and is known to induce proliferation, migration, differentiation, apoptotic cell death, inflammation, and angiogenesis. These physiological processes are induced by the binding of TWEAK to fibroblast growth factor-inducible 14 (Fn14), a highly inducible cell-surface receptor that is linked to several intracellular signaling pathways, including the nuclear factor-κB (NF-κB) pathway. This review discusses the role of the TWEAK-Fn14 axis in several rheumatic diseases and the potential therapeutic benefits of modulation of the TWEAK-Fn14 pathway.


Assuntos
Humanos , Artrite Reumatoide , Citocina TWEAK , Lúpus Eritematoso Sistêmico , Receptores do Fator de Necrose Tumoral , Fisiologia , Doenças Reumáticas , Escleroderma Sistêmico , Receptor de TWEAK , Fatores de Necrose Tumoral , Fisiologia
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