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Results suggested that TNFSF15 (rs3810936 and rs4979462) SNPs may confer susceptibility to systemic lupus erythematosus (SLE) risk, which were significantly associated with the clinical phenotypes of SLE.
Three alternatively spliced isoforms of VEGI, VEGI174, VEGI192 and VEGI251 have been documented. This study investigated the effects of VEGI174 and its functional domains (V7 and V8) on epithelialmesenchymal transition (EMT (show ITK Proteins)) in renal cell carcinoma (show MOK Proteins) (RCC (show XRCC1 Proteins)) cells in vitro. Overexpression of VEGI174, V7 or V8 inhibited EMT (show ITK Proteins).
Results provide evidence that variance within TNFSF15 has the potential to affect cytokine expression across a range of tissues and thereby contribute to protection from infectious diseases such as leprosy, while increasing the risk of immune-mediated diseases including Crohn's disease and primary biliary cholangitis.
single variant analysis detected a previously unreported psoriasis risk locus at TNFSF15 (rs6478108)
the DR3 (show TNFRSF25 Proteins)/TL1A pathway directly enhances human OC formation and resorptive activity, controlling expression and activation of CCL3 (show CCL3 Proteins) and MMP-9 (show MMP9 Proteins).
the blocking of tumor necrosis factor receptor 2 (TNFR2 (show TNFRSF1B Proteins)) decreased TL1A-stimulated IL-6 (show IL6 Proteins) production by rheumatoid arthritis fibroblast-like synoviocytes.
Distinct but overlapping TNFSF15 haplotypes were demonstrated in diverticulitis patients versus healthy controls when compared with the known Crohn's risk haplotype suggesting similar but distinct genetic predispositions. This study strengthens the role for a genetic predisposition to diverticulitis that involves the TNFSF15 gene.
TL1A differentially induces expression of TH17 effector cytokines IL-17 (show IL17A Proteins), -9, and -22 and provides a potential target for therapeutic intervention in TH17-driven chronic inflammatory diseases.
Our findings indicate that VEGI174 prevents progression and tumor metastasis through inhibiting epithelial-mesenchymal transition (EMT (show ITK Proteins)) in renal cell carcinoma (show MOK Proteins) (RCC (show XRCC1 Proteins)) in vivo. This may provide a new approach for the treatment of RCC (show XRCC1 Proteins)
Data suggest that human regulatory T-lymphocytes express DR3 (show TNFRSF25 Proteins) and demonstrate DR3 (show TNFRSF25 Proteins)/TL1A-mediated activation of signaling via MAP kinases and NFkappaB (show NFKB1 Proteins). (DR3 (show TNFRSF25 Proteins) = death receptor 3 (show TNFRSF25 Proteins); TL1A/TNFSF15 = tumor necrosis factor (show TNF Proteins) [ligand] superfamily, member 15)
ATF3 (show ATF3 Proteins) protects against LPS (show TLR4 Proteins)-induced acute lung injury by inhibiting TL1A expression.
This work describes both a novel function and essential requirement for the DR3 (show TNFRSF25 Proteins)/TL1A pathway in acute, resolving, and chronic inflammation in the peritoneal cavity.
this study shows that TL1A-/- mice are more susceptible to dextran sodium sulfate colitis
These data demonstrated a direct role for TL1A-DR3 (show TNFRSF25 Proteins) signaling in tissue fibrosis and that modulation of TL1A-DR3 (show TNFRSF25 Proteins) signaling could inhibit gut (show GUSB Proteins) fibrosis.
these data identify TL1A-DR3 (show TNFRSF25 Proteins) interactions as a novel pathway that promotes Th9 differentiation and pathogenicity. TL1A may be a potential therapeutic target in diseases dependent on IL-9 (show IL9 Proteins).
TL1A induces NF-kappaB (show NFKB1 Proteins) activation in EC in renal and cardiac tissue from wild type but not DR3 (show TNFRSF25 Proteins) knock-out mice.
TL1A deficiency impacts on the gut (show GUSB Proteins) microbial composition and the mucosal immune system, especially the intraepithelial TCRgammadelta(+) T-cell subset, and that TL1A is involved in the establishment of adipose tissue.
Our data demonstrate a key role for TL1A in promoting ILC2s at mucosal barriers.
TNFSF15 inhibits vasculogenesis by regulating relative levels of membrane-bound and soluble isoforms of VEGF receptor (show FLT1 Proteins) 1.
Both in supernatant and as purified fusion protein, TL1A-Ig binds to TNFRSF25 (show TNFRSF25 Proteins) transfected--but not untransfected--P815 tumor cells as determined by flow cytometry.
The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein is abundantly expressed in endothelial cells, but is not expressed in either B or T cells. The expression of this protein is inducible by TNF and IL-1 alpha. This cytokine is a ligand for receptor TNFRSF25 and decoy receptor TNFRSF21/DR6. It can activate NF-kappaB and MAP kinases, and acts as an autocrine factor to induce apoptosis in endothelial cells. This cytokine is also found to inhibit endothelial cell proliferation, and thus may function as an angiogenesis inhibitor. Two transcript variants encoding different isoforms have been found for this gene.
tumor necrosis factor ligand superfamily member 15
, vascular endothelial growth inhibitor
, tocopherol (alpha) transfer protein-like
, TNF ligand-related molecule 1
, TNF superfamily ligand TL1A
, vascular endothelial cell growth inhibitor
, vascular endothelial growth inhibitor-192A
, bM20K13.3 (tumor necrosis factor (ligand) superfamily, member 15)