![]() ![]() "TWEAK/Fn14 axis: the current paradigm of tissue injury-inducible function in the midst of complexities". "TWEAK attenuates the transition from innate to adaptive immunity". ^ Maecker H, Varfolomeev E, Kischkel F, Lawrence D, LeBlanc H, Lee W, Hurst S, Danilenko D, Li J, Filvaroff E, Yang B, Daniel D, Ashkenazi A (December 2005).^ a b "Entrez Gene: TNFSF12 tumor necrosis factor (ligand) superfamily, member 12"."Identification of a ligand for the death-domain-containing receptor Apo3". ^ Marsters SA, Sheridan JP, Pitti RM, Brush J, Goddard A, Ashkenazi A (April 1998)."TWEAK, a new secreted ligand in the tumor necrosis factor family that weakly induces apoptosis". ^ a b Chicheportiche Y, Bourdon PR, Xu H, Hsu YM, Scott H, Hession C, Garcia I, Browning JL (December 1997).National Center for Biotechnology Information, U.S. In chronic liver disease, for example, TWEAK expression is enhanced and causes hepatic stellate cells, which are key regulators of liver fibrosis, to proliferate. Clinical significance Įxcessive activation of the TWEAK pathway in chronic injury has been described to promote pathological tissue changes including chronic inflammation, fibrosis and angiogenesis. This cytokine is also found to promote proliferation and migration of endothelial cells, and thus acts as a regulator of angiogenesis. TWEAK can induce apoptosis via multiple pathways of cell death in a cell type-specific manner. Leukocytes are the main source of TWEAK including human resting and activated monocytes, dendritic cells and natural killer cells. This cytokine has overlapping signaling functions with TNF, but displays a much wider tissue distribution. This protein is a ligand for the FN14/ TWEAKR receptor. The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. Tumor necrosis factor ligand superfamily member 12 also known as TNF-related weak inducer of apoptosis (TWEAK) is a protein that in humans is encoded by the TNFSF12 gene. regulation of signaling receptor activity.positive regulation of extrinsic apoptotic signaling pathway.tumor necrosis factor-mediated signaling pathway.positive regulation of protein catabolic process.positive regulation of endothelial cell proliferation. ![]()
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