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anti-Human 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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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.
TWEAK upregulated the expression of Fn14 (show TNFRSF12A Antibodies).
Fn14 (show TNFRSF12A Antibodies) plays a protective role during the acute stages of intestinal inflammation, and its absence promotes the development of colitis-associated cancer.
Fn14 (show TNFRSF12A Antibodies).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 (show DDX3X Antibodies) (Fn14 (show TNFRSF12A Antibodies)) signaling axis, which could potentially be developed as a new therapeutic agent for treatment of glioblastoma (GBM) patients.
soluble Fn14 (show TNFRSF12A Antibodies) 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 (show MMP9 Antibodies) was induced by TWEAK in LX-2 cells, which enhanced the migration. Furthermore, our findings showed that TWEAK upregulated the phosphorylation of IkappaBalpha (show NFKBIA Antibodies) and p65 (show GORASP1 Antibodies) protein to increase MMP9 (show MMP9 Antibodies) expression in LX-2 cells.
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 (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.
TWEAK/Fn14 (show TNFRSF12A Antibodies) signaling represses PGC-1alpha (show PPARGC1A Antibodies) expression during acute kidney injury through activation of canonical NF-kappaB (show NFKB1 Antibodies) pathways and epigenetic mechanisms including histone deacetylation on NF-kappaB (show NFKB1 Antibodies)-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 (show TNFRSF12A Antibodies) 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 (show CD163 Antibodies) functions as a decoy receptor for TWEAK, to regulate TWEAK-induced activation of canonical nuclear factor-kappaB and Notch (show NOTCH1 Antibodies) signalling necessary for myogenic progenitor cell proliferation.
TWEAK/Fn14 (show TNFRSF12A Antibodies) interactions play an important role in the pathogenesis of neuropsychiatric lupus by increasing the accumulation of inflammatory cells in the choroid plexus, disrupting blood brain barrier integrity, and increasing neuronal damage
Tweak regulates astrogliosis, microgliosis and skeletal muscle atrophy in a mouse model of amyotrophic lateral sclerosis
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