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Proinflammatory activity of TWEAK on human dermal fibroblasts and synoviocytes: blocking and enhancing effects of anti-TWEAK monoclonal antibodies.
Chicheportiche Y, Chicheportiche R, Sizing I, Thompson J, Benjamin CB, Ambrose C, Dayer JM
Arthritis Res 2002, 4:126-33
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TWEAK induces liver progenitor cell proliferation.
Jakubowski A, Ambrose C, Parr M, Lincecum JM, Wang MZ, Zheng TS, Browning B, Michaelson JS, Baetscher M, Baestcher M, Wang B, Bissell DM, Burkly LC
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The Fn14 cytoplasmic tail binds tumour-necrosis-factor-receptor-associated factors 1, 2, 3 and 5 and mediates nuclear factor-kappaB activation.
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TWEAK binding to the Fn14 cysteine-rich domain depends on charged residues located in both the A1 and D2 modules.
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A soluble Fn14-Fc decoy receptor reduces infarct volume in a murine model of cerebral ischemia.
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TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration.
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Proinflammatory effects of tumour necrosis factor-like weak inducer of apoptosis (TWEAK) on human gingival fibroblasts.
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Molecular subsets in the gene expression signatures of scleroderma skin.
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