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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
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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
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Human Polyclonal TNFSF12 Primary Antibody for IHC (p), WB - ABIN541270
Lynch, Wang, Lund, Chen, Leal, Wiley: TWEAK induces angiogenesis and proliferation of endothelial cells. in The Journal of biological chemistry 1999
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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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These results demonstrate that TWEAK/Fn14 signaling contributes to Graves' orbitopathy (GO) pathogenesis. Moreover, serum TWEAK level is a potential diagnostic biomarker for inflammatory GO, and modulating TWEAK activity may be an effective therapeutic strategy for suppressing inflammation and tissue remodeling in GO.
full-length TWEAK stimulated IL-8 gene expression in endothelial EA.hy.926 cells, whereas the triple-deletion mutant lost much of this activity, suggesting that the TWEAK-AGE interaction sites overlap with the region needed to exert normal function of TWEAK.
Serum levels of soluble TWEAK were decreased in healthy controls and normoalbuminuria when compared to patients with diabetic nephropathy.
The truncated DR3 protein product lacks the death domain and forms a heterotrimer complex with wildtype DR3 that dominant-negatively inhibits ligand-induced apoptosis in lymphocytes.
No clinical neuropsychiatric manifestations could be attributed to impaired integrity of the blood-brain barrier, or to TWEAK levels in cerebrospinal fluid or serum in systemic lupus erythematosus and primary Sjogren's syndrome.
TWEAK/Fn14 interaction induces proliferation and migration in human airway smooth muscle cells via activating the NF-kappaB pathway
In lupus nephritis, urinary MCP-1 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 contributes to endothelial dysfunction through modulation of reactive oxygen species (ROS), and mitochondrial ROS.
Expression of the TWEAK-Fn14 axis was upregulated in patients with autoimmune thyroid disease and might play a role in the pathogenesis of autoimmune thyroid disease.
we show that sTWEAK levels are lower in HIV-infected patients compared to uninfected participants. Our findings also suggest that sTWEAK might have a role in the pathogenesis of atherosclerosis in patients with HIV.
TWEAK:Fn14 binding activates non-canonical NF-kappaB signaling in prostate cancer cells, stimulating cell invasiveness.
The results suggest that TWEAK/Fn14 interaction directly favors inorganic phosphate-induced vascular smooth muscle cells calcification by activation of both canonical and non-canonical NF-kappaB 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 expression and cellular adherence, involving the activation of ERK and NF-kappaB pathways. TWEAK may serve as a biomarker or therapeutic target of BP.
TWEAK upregulated the expression of Fn14.
Fn14 plays a protective role during the acute stages of intestinal inflammation, and its absence promotes the development of colitis-associated cancer.
Fn14.TRAIL can be converted into a highly effective TRAIL oligomer upon binding to TWEAK which induces lymphoblast apoptosis.
TWEAK upregulates CD74 and its ligands MIF and DDT in renal tubular cells.
TWEAK is a critical contributor to skin inflammation and a possible therapeutic target in atopic dermatitis and psoriasis
A Nec-1-sensitive cell death pathway, presumably driven by an inflammatory response involving TWEAK/Fn14 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-200bc/429 cluster alleviates inflammation in IgA nephropathy by targeting TWEAK/Fn14
TWEAK:Fn14 binding activates non-canonical NF-kappaB signaling in B16 melanoma cells, inhibiting cell invasiveness.
TWEAK/Fn14 signalling is important in the pathogenesis of ultraviolet B-induced cutaneous disease manifestations in the MRL/lpr model of lupus.
Disruption of the TWEAK/Fn14 pathway affects several interconnected pathways, including those associated with IL-13, IL-33, 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 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 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 signaling pathway, and phosphorylation of Smad2 and p38 MAPK proteins was also involved in this signaling pathway.
TWEAK/Fn14 signaling represses PGC-1alpha expression during acute kidney injury through activation of canonical NF-kappaB pathways and epigenetic mechanisms including histone deacetylation on NF-kappaB-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 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 functions as a decoy receptor for TWEAK, to regulate TWEAK-induced activation of canonical nuclear factor-kappaB and Notch signalling necessary for myogenic progenitor cell proliferation.
TWEAK/Fn14 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 results demonstrated that the expression levels of TWEAK and p-p38 MAPK increased in the periprosthetic interface membrane tissues and the RAW cells stimulated with Ti particles
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