Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024141 (systemic lupus erythematosus)
44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

TNF-like weak inducer of apoptosis (TWEAK) is a member of the TNFSF ligands, initially synthesized as a type II transmembrane protein. TWEAK signaling occurs via binding to Fn14, a type I transmembrane receptor belonging to the TNF receptor superfamily. TWEAK/Fn14 activation controls several cellular responses, including proliferation, angiogenesis, induction of inflammatory cytokines. Studies have indicated that expression of TWEAK/Fn14 was dysregulated in autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, inflammatory bowel disease. Functional analysis suggested that TWEAK/Fn14 may play an important role in the development of these diseases. In this review, we discuss the TWEAK/Fn14 pathway and its significant role in autoimmune disorders. The information obtained may lead to a better understanding of the insights into TWEAK/Fn14 in these autoimmune diseases.
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PMID:Role of the TWEAK/Fn14 pathway in autoimmune diseases. 2665 91