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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
The reduced levels of sTWEAK with progression of Hashimoto's Thyroiditis and the significant correlation between the sTWEAK levels and anti-TPO (show THPO Proteins) found in this study suggest that sTWEAK plays an active role in chronic inflammation in the pathogenesis of Hashimoto's Thyroiditis and in the progression of autoimmunity.
Serum TWEAK might be a serologic biomarker candidate that reflects disease activity and renal involvement in patients with SLE
TWEAK/Fn14 (show TNFRSF12A Proteins) activation induces keratinocyte proliferation under psoriatic inflammation
Heart failure with reduced ejection fraction (HF-REF (show THOC4 Proteins)) patients present increased sTWEAK and sCD163 (show CD163 Proteins) levels as well as sTWEAK/sCD163 (show CD163 Proteins) ratio when compared to healthy subjects, however CHF itself appears to be associated with down-regulation of sTWEAK.
The results demonstrated that vitreous fluid from patients with PDR had higher levels of TWEAK and Fn14 than that from T2DM patients without PDR, thus suggesting an important regulatory role of TWEAK/Fn14 signaling in the pathogenesis of PDR.
The main determinant of nitroglycerin-mediated dilation was sTWEAK. In addition, decreased nitroglycerin-mediated dilation was associated with higher systolic blood pressure and pulse pressure. The main determinant of FMD (show FLNA Proteins) was Kt/V. Increased flow-mediated dilation was associated with better dialysis efficiency and high total cholesterol and LDL-cholesterol.
TWEAK levels are slightly elevated in CSF (show CSF2 Proteins) in systemic lupus erythematosus patients compared with non-autoimmune controls, irrespective of the presence of neuropsychiatric disease manifestations. TWEAK levels in serum and CSF (show CSF2 Proteins) do not seem to be a useful biomarker of CNS involvement in SLE.
Study demonstrates that soluble TWEAK is decreased in patients with preeclampsia compared to healthy pregnant women.
High TWEAK levels are associated with Inflammatory Bowel Disease etiopathogenesis.
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
TWEAK/Fn14 (show TNFRSF12A Proteins) signaling represses PGC-1alpha expression during acute kidney injury through activation of canonical NF-kappaB (show NFKB1 Proteins) pathways and epigenetic mechanisms including histone deacetylation on NF-kappaB (show NFKB1 Proteins)-binding sites.
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.
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