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Human TNFSF12 Protein expressed in Escherichia coli (E. coli) - ABIN935856
Han, Mekasha, Ingalls: Fibroblast growth factor-inducible 14 (Fn14) is expressed in the lower genital tract and may play a role in amplifying inflammation during infection. in Journal of reproductive immunology 2010
TWEAK/Fn14 (zeige TNFRSF12A Proteine) interaction induces proliferation and migration in human airway smooth muscle cells via activating the NF-kappaB (zeige NFKB1 Proteine) pathway
In lupus nephritis, urinary MCP-1 (zeige CCL2 Proteine) and TWEAK possess higher correlation coefficients with renal damage and larger areas under ROC curves than other markers for rapid discrimination of severe disease.
Airway TWEAK may play a role in small airway inflammation especially in children with non-eosinophilic asthma.
Results suggest that TWEAK expression is relatively low in non-small cell lung cancer tissues and not associated with relapse-free survival rate. In addition, TWEAK is found not to promote cell proliferation and migration.
TWEAK/Fn14 (zeige TNFRSF12A Proteine) contributes to endothelial dysfunction through modulation of reactive oxygen species (ROS (zeige ROS1 Proteine)), and mitochondrial ROS (zeige ROS1 Proteine).
Expression of the TWEAK-Fn14 (zeige TNFRSF12A Proteine) axis was upregulated in patients with autoimmune thyroid disease and might play a role in the pathogenesis of autoimmune thyroid disease.
TWEAK:Fn14 binding activates non-canonical NF-kappaB (zeige NFKB1 Proteine) signaling in prostate cancer cells, stimulating cell invasiveness.
The results suggest that TWEAK/Fn14 (zeige TNFRSF12A Proteine) interaction directly favors inorganic phosphate-induced vascular smooth muscle cells calcification by activation of both canonical and non-canonical NF-kappaB (zeige NFKB1 Proteine) pathways.
during psoriatic arthritis (1) serum TWEAK was up regulated and (2) TWEAK-binding autoantibodies are generated.
Plasma TWEAK levels do not reflect disease activity or the grade of inflammation in patients with newly diagnosed inflammatory bowel disease.
A Nec-1 (zeige PCSK1 Proteine)-sensitive cell death pathway, presumably driven by an inflammatory response involving TWEAK/Fn14 (zeige TNFRSF12A Proteine) to an initial wave of cell death, appears to be responsible for amplification of the tubular cell death response and for persistence of acute kidney injury
Our results illustrate a novel regulatory role of TWEAK, in which its activity positively regulates type I IFN pathway in lupus nephritis (LN) based on preclinical models. Our findings suggest TWEAK could act as a critical target in preventing renal damage in patients with LN.
this paper shows that miR (zeige MLXIP Proteine)-200bc/429 cluster alleviates inflammation in IgA nephropathy by targeting TWEAK/Fn14 (zeige TNFRSF12A Proteine)
TWEAK:Fn14 binding activates non-canonical NF-kappaB (zeige NFKB1 Proteine) signaling in B16 melanoma cells, inhibiting cell invasiveness.
TWEAK/Fn14 (zeige TNFRSF12A Proteine) signalling is important in the pathogenesis of ultraviolet B-induced cutaneous disease manifestations in the MRL/lpr (zeige FAS Proteine) model of lupus.
Disruption of the TWEAK/Fn14 (zeige TNFRSF12A Proteine) pathway affects several interconnected pathways, including those associated with IL-13 (zeige IL13 Proteine), IL-33 (zeige IL33 Proteine), and IL-13Ralpha2, to attenuate 5-fluorouracil-induced intestinal side effects.
TWEAK promotes migration and invasion in murine embryonic fibroblasts through a mechanism dependent on ERKs activation and Fibulin 3 (zeige FBLN3 Proteine) down-regulation.
These results implicate TWEAK as a potential molecular target for treatment or prevention of inflammatory arthritis and autoimmune diseases such as rheumatoid arthritis.
soluble Fn14 (zeige TNFRSF12A Proteine) may serve as a potential biomarker for both acute and chronic kidney diseases.
Findings suggest that TWEAK may contribute to chronic renal changes and renal fibrosis by activating TGF-beta1 (zeige TGFB1 Proteine) signaling pathway, and phosphorylation of Smad2 (zeige SMAD2 Proteine) and p38 MAPK (zeige MAPK14 Proteine) proteins was also involved in this signaling pathway.
The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein is a ligand for the FN14/TWEAKR receptor. This cytokine has overlapping signaling functions with TNF, but displays a much wider tissue distribution. This cytokine, which exists in both membrane-bound and secreted forms, can induce apoptosis via multiple pathways of cell death in a cell type-specific manner. This cytokine is also found to promote proliferation and migration of endothelial cells, and thus acts as a regulator of angiogenesis. Alternative splicing results in multiple transcript variants. Some transcripts skip the last exon of this gene and continue into the second exon of the neighboring TNFSF13 gene\; such read-through transcripts are contained in GeneID 407977, TNFSF12-TNFSF13.
, APO3/DR3 ligand
, TNF-related WEAK inducer of apoptosis
, tumor necrosis factor ligand superfamily member 12
, tumor necrosis factor superfamily member 12
, TNF-related weak inducer of apoptosis