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Human TNFSF12 Protein expressed in Escherichia coli (E. coli) - ABIN2666450
Bover, Cardó-Vila, Kuniyasu, Sun, Rangel, Takeya, Aggarwal, Arap, Pasqualini: A previously unrecognized protein-protein interaction between TWEAK and CD163: potential biological implications. in Journal of immunology (Baltimore, Md. : 1950) 2007
Show all 7 references for ABIN2666450
Human TNFSF12 Protein expressed in Escherichia coli (E. coli) - ABIN2667599
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
Show all 6 references for ABIN2667599
Mouse (Murine) TNFSF12 Protein expressed in Human Cells - ABIN2007454
Campbell, Michaelson, Burkly, Putterman: The role of TWEAK/Fn14 in the pathogenesis of inflammation and systemic autoimmunity. in Frontiers in bioscience : a journal and virtual library 2004
Show all 2 references for ABIN2007454
Rat (Rattus) TNFSF12 Protein expressed in Human Cells - ABIN2009223
Lynch, Wang, Lund, Chen, Leal, Wiley: TWEAK induces angiogenesis and proliferation of endothelial cells. in The Journal of biological chemistry 1999
Show all 2 references for ABIN2009223
Human TNFSF12 Protein expressed in Escherichia coli (E. coli) - ABIN935856
Han, Mekasha, Ingalls: Fibroblast growth factor-inducible 14 (Fn14) is expressed in the lower genital tract and may play a role in amplifying inflammation during infection. in Journal of reproductive immunology 2010
Data indicate that serum levels of tumour necrosis factor (TNF (show TNF Proteins))-like weak inducer of apoptosis (TWEAK) were significantly higher in psoriasis patients compared to controls.
We identified five new biomarkers: GDF15 (show GDF15 Proteins), osteonectin (show SPARC Proteins), TRAP5, TWEAK, and YKL40 (show CHI3L1 Proteins) as being promising markers for monitoring bone metastases.
TWEAK/Fn14 (show TNFRSF12A Proteins) interaction promotes oxidative stress through NADPH oxidase (show NOX1 Proteins) 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 Proteins) have synergistic effects in EMT (show ITK Proteins) and may contribute to chronic airway changes and remodeling.
TWEAK induces noncanonical NF-kappaB (show NFKB1 Proteins) signaling and signal-specific regulation of NIK (show MAP3K14 Proteins) mRNA expression.
This review describes the interactions between Tweak and Fn14 (show TNFRSF12A Proteins) 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 Proteins) axis.
TWEAK-Fn14 (show TNFRSF12A Proteins) axis may be involved in the pathogenesis of polymyositis and dermatomyositis
results revealed that TWEAK and Fn14 (show TNFRSF12A Proteins) 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 Proteins) functions as a decoy receptor for TWEAK, to regulate TWEAK-induced activation of canonical nuclear factor-kappaB and Notch (show NOTCH1 Proteins) signalling necessary for myogenic progenitor cell proliferation.
TWEAK/Fn14 (show TNFRSF12A Proteins) 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 Proteins) increased in the periprosthetic interface membrane tissues and the RAW cells stimulated with Ti particles
TWEAK/Fn14 (show TNFRSF12A Proteins) signaling is strongly implicated in the pathogenesis of the cutaneous manifestations in the MRL/lpr (show FAS Proteins) model of spontaneous lupus in mice.
synergistic activation of canonical NF-kappaB (show NFKB1 Proteins) by TWEAK and TNF-alpha (show TNF Proteins) 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 Proteins) resistance, and metabolic dysfunction.
TWEAK/Fn14 (show TNFRSF12A Proteins) 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