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anti-Human TNFSF12 Antibodies:
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Human Polyclonal TNFSF12 Primary Antibody for EIA, IHC (p) - ABIN501094
Lynch, Wang, Lund, Chen, Leal, Wiley: TWEAK induces angiogenesis and proliferation of endothelial cells. in The Journal of biological chemistry 1999
Show all 5 references for ABIN501094
Dog (Canine) Polyclonal TNFSF12 Primary Antibody for WB - ABIN2774826
Park, Chung, Jung, Park, Lee: Relationship of serum TWEAK level to cytokine level, disease activity, and response to anti-TNF treatment in patients with rheumatoid arthritis. in Scandinavian journal of rheumatology 2008
Data indicate that serum levels of tumour necrosis factor (TNF (show TNF Antibodies))-like weak inducer of apoptosis (TWEAK) were significantly higher in psoriasis patients compared to controls.
We identified five new biomarkers: GDF15 (show GDF15 Antibodies), osteonectin (show SPARC Antibodies), TRAP5, TWEAK, and YKL40 (show CHI3L1 Antibodies) as being promising markers for monitoring bone metastases.
TWEAK/Fn14 (show TNFRSF12A Antibodies) interaction promotes oxidative stress through NADPH oxidase (show NOX1 Antibodies) activation in macrophages.
HIV-associated lipodystrophy syndrome is associated with decreased serum TWEAK levels.
Suggest that the pro-inflammatory cytokine TWEAK and TGF-beta1 (show TGFB1 Antibodies) have synergistic effects in EMT (show ITK Antibodies) and may contribute to chronic airway changes and remodeling.
TWEAK induces noncanonical NF-kappaB (show NFKB1 Antibodies) signaling and signal-specific regulation of NIK (show MAP3K14 Antibodies) mRNA expression.
This review describes the interactions between Tweak and Fn14 (show TNFRSF12A Antibodies) and how they play critical roles in osteoclast differentiation.
HPV16 infection keratinocytes causes switch of apoptosis to proliferative phase under TWEAK interaction..
The first human data to show a transient activation of the TWEAK-Fn14 (show TNFRSF12A Antibodies) axis.
TWEAK-Fn14 (show TNFRSF12A Antibodies) axis may be involved in the pathogenesis of polymyositis and dermatomyositis
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 results demonstrated that the expression levels of TWEAK and p-p38 MAPK (show MAPK14 Antibodies) increased in the periprosthetic interface membrane tissues and the RAW cells stimulated with Ti particles
TWEAK/Fn14 (show TNFRSF12A Antibodies) signaling is strongly implicated in the pathogenesis of the cutaneous manifestations in the MRL/lpr (show FAS Antibodies) model of spontaneous lupus in mice.
synergistic activation of canonical NF-kappaB (show NFKB1 Antibodies) by TWEAK and TNF-alpha (show TNF Antibodies) is critical for the induction of inflammatory tissue damage in acute inflammation.
Elevated levels of TWEAK in skeletal muscle promote visceral obesity, insulin (show INS Antibodies) resistance, and metabolic dysfunction.
TWEAK/Fn14 (show TNFRSF12A Antibodies) pathway instrumental in the pathogenesis of spontaneous lupus nephritis
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