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anti-Human TNFSF12 Antibodies:
anti-Mouse (Murine) TNFSF12 Antibodies:
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Human Monoclonal TNFSF12 Primary Antibody for FACS - ABIN1176948
Llinàs, Lázaro, de Salort, Matesanz-Isabel, Sintes, Engel: Expression profiles of novel cell surface molecules on B-cell subsets and plasma cells as analyzed by flow cytometry. in Immunology letters 2010
Show all 5 Pubmed References
Human Polyclonal TNFSF12 Primary Antibody for ELISA, IHC - ABIN4363574
Ruiz-Andres, Suarez-Alvarez, Sánchez-Ramos, Monsalve, Sanchez-Niño, Ruiz-Ortega, Egido, Ortiz, Sanz: The inflammatory cytokine TWEAK decreases PGC-1α expression and mitochondrial function in acute kidney injury. in Kidney international 2016
Show all 2 Pubmed References
Human Monoclonal TNFSF12 Primary Antibody for ELISA - ABIN2477010
Chicheportiche, Bourdon, Xu, Hsu, Scott, Hession, Garcia, Browning: TWEAK, a new secreted ligand in the tumor necrosis factor family that weakly induces apoptosis. in The Journal of biological chemistry 1998
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In lupus nephritis, urinary MCP-1 (show CCL2 Antibodies) 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 (show TNFRSF12A Antibodies) contributes to endothelial dysfunction through modulation of reactive oxygen species (ROS (show ROS1 Antibodies)), and mitochondrial ROS (show ROS1 Antibodies).
Expression of the TWEAK-Fn14 (show TNFRSF12A Antibodies) 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 (show NFKB1 Antibodies) signaling in prostate cancer cells, stimulating cell invasiveness.
The results suggest that TWEAK/Fn14 (show TNFRSF12A Antibodies) interaction directly favors inorganic phosphate-induced vascular smooth muscle cells calcification by activation of both canonical and non-canonical NF-kappaB (show NFKB1 Antibodies) 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 (show COL17A1 Antibodies) expression and cellular adherence, involving the activation of ERK (show EPHB2 Antibodies) and NF-kappaB (show NFKB1 Antibodies) pathways. TWEAK may serve as a biomarker or therapeutic target of BP.
A Nec-1 (show PCSK1 Antibodies)-sensitive cell death pathway, presumably driven by an inflammatory response involving TWEAK/Fn14 (show TNFRSF12A Antibodies) 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 (show MLXIP Antibodies)-200bc/429 cluster alleviates inflammation in IgA (show IgA Antibodies) nephropathy by targeting TWEAK/Fn14 (show TNFRSF12A Antibodies)
TWEAK:Fn14 binding activates non-canonical NF-kappaB (show NFKB1 Antibodies) signaling in B16 melanoma cells, inhibiting cell invasiveness.
TWEAK/Fn14 (show TNFRSF12A Antibodies) signalling is important in the pathogenesis of ultraviolet B-induced cutaneous disease manifestations in the MRL/lpr (show FAS Antibodies) model of lupus.
Disruption of the TWEAK/Fn14 (show TNFRSF12A Antibodies) pathway affects several interconnected pathways, including those associated with IL-13 (show IL13 Antibodies), IL-33 (show IL33 Antibodies), 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 (show FBLN3 Antibodies) 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 (show TNFRSF12A Antibodies) 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 (show TGFB1 Antibodies) signaling pathway, and phosphorylation of Smad2 (show SMAD2 Antibodies) and p38 MAPK (show MAPK14 Antibodies) 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