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anti-Human TNFSF12 Antikörper:
anti-Mouse (Murine) TNFSF12 Antikörper:
anti-Rat (Rattus) TNFSF12 Antikörper:
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Human Monoclonal TNFSF12 Primary Antibody für 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
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Human Polyclonal TNFSF12 Primary Antibody für 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
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Human Monoclonal TNFSF12 Primary Antibody für 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 (zeige TNFRSF12A Antikörper) interaction directly favors inorganic phosphate-induced vascular smooth muscle cells calcification by activation of both canonical and non-canonical NF-kappaB (zeige NFKB1 Antikörper) 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 Antikörper) expression and cellular adherence, involving the activation of ERK (zeige EPHB2 Antikörper) and NF-kappaB (zeige NFKB1 Antikörper) pathways. TWEAK may serve as a biomarker or therapeutic target of BP.
TWEAK upregulated the expression of Fn14 (zeige TNFRSF12A Antikörper).
Fn14 (zeige TNFRSF12A Antikörper) plays a protective role during the acute stages of intestinal inflammation, and its absence promotes the development of colitis-associated cancer.
Fn14 (zeige TNFRSF12A Antikörper).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 Antikörper) (Fn14 (zeige TNFRSF12A Antikörper)) signaling axis, which could potentially be developed as a new therapeutic agent for treatment of glioblastoma (GBM) patients.
soluble Fn14 (zeige TNFRSF12A Antikörper) 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 Antikörper) 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 Antikörper) and p65 (zeige GORASP1 Antikörper) protein to increase MMP9 (zeige MMP9 Antikörper) expression in LX-2 cells.
TWEAK promotes migration and invasion in murine embryonic fibroblasts through a mechanism dependent on ERKs activation and Fibulin 3 (zeige FBLN3 Antikörper) 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 Antikörper) signaling pathway, and phosphorylation of Smad2 (zeige SMAD2 Antikörper) and p38 MAPK (zeige MAPK14 Antikörper) proteins was also involved in this signaling pathway.
TWEAK/Fn14 (zeige TNFRSF12A Antikörper) signaling represses PGC-1alpha (zeige PPARGC1A Antikörper) expression during acute kidney injury through activation of canonical NF-kappaB (zeige NFKB1 Antikörper) pathways and epigenetic mechanisms including histone deacetylation on NF-kappaB (zeige NFKB1 Antikörper)-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 Antikörper) 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 Antikörper) functions as a decoy receptor for TWEAK, to regulate TWEAK-induced activation of canonical nuclear factor-kappaB and Notch (zeige NOTCH1 Antikörper) signalling necessary for myogenic progenitor cell proliferation.
TWEAK/Fn14 (zeige TNFRSF12A Antikörper) 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
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