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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
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.
TWEAK may contribute to the pathogenesis of BP by reducing BP180 (zeige COL17A1 Proteine) expression and cellular adherence, involving the activation of ERK (zeige EPHB2 Proteine) and NF-kappaB (zeige NFKB1 Proteine) pathways. TWEAK may serve as a biomarker or therapeutic target of BP.
TWEAK upregulated the expression of Fn14 (zeige TNFRSF12A Proteine).
Fn14 (zeige TNFRSF12A Proteine) plays a protective role during the acute stages of intestinal inflammation, and its absence promotes the development of colitis-associated cancer.
Fn14 (zeige TNFRSF12A Proteine).TRAIL can be converted into a highly effective TRAIL oligomer upon binding to TWEAK which induces lymphoblast apoptosis.
Data show that aurintricarboxylic acid (ATA) targets the TNF-related WEAK inducer of apoptosis (TWEAK)-fibroblast growth factor-inducible 14 (zeige DDX3X Proteine) (Fn14 (zeige TNFRSF12A Proteine)) signaling axis, which could potentially be developed as a new therapeutic agent for treatment of glioblastoma (GBM) patients.
soluble Fn14 (zeige TNFRSF12A Proteine) may serve as a potential biomarker for both acute and chronic kidney diseases.
The result of transwell assay revealed that TWEAK promoted LX-2 migration. Subsequently, our data testified that the expression and activity of MMP9 (zeige MMP9 Proteine) was induced by TWEAK in LX-2 cells, which enhanced the migration. Furthermore, our findings showed that TWEAK upregulated the phosphorylation of IkappaBalpha (zeige NFKBIA Proteine) and p65 (zeige GORASP1 Proteine) protein to increase MMP9 (zeige MMP9 Proteine) expression in LX-2 cells.
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.
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.
TWEAK/Fn14 (zeige TNFRSF12A Proteine) signaling represses PGC-1alpha expression during acute kidney injury through activation of canonical NF-kappaB (zeige NFKB1 Proteine) pathways and epigenetic mechanisms including histone deacetylation on NF-kappaB (zeige NFKB1 Proteine)-binding sites.
These findings suggest that TWEAK signaling might be an aspect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine -mediated neuropathology and be involved in the overall neurodegenerative pathology of Parkinson's disease
results revealed that TWEAK and Fn14 (zeige TNFRSF12A Proteine) are expressed by uterine natural killer cells in pregnant mice
studies show that signaling via TWEAK is deleterious to muscle in RNA toxicity and support the demonstrated utility of anti-TWEAK therapeutics.
During ischaemia, soluble CD163 (zeige CD163 Proteine) functions as a decoy receptor for TWEAK, to regulate TWEAK-induced activation of canonical nuclear factor-kappaB and Notch (zeige NOTCH1 Proteine) signalling necessary for myogenic progenitor cell proliferation.
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