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anti-Human TNFSF15 Antikörper:
anti-Mouse (Murine) TNFSF15 Antikörper:
anti-Rat (Rattus) TNFSF15 Antikörper:
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Human Polyclonal TNFSF15 Primary Antibody für WB - ABIN2476844
Tinkanen, Kujansuu: Doppler ultrasound studies in pelvic inflammatory disease. in Gynecologic and obstetric investigation 1993
Show all 3 Pubmed References
Human Polyclonal TNFSF15 Primary Antibody für IF (p), IHC (p) - ABIN709556
?lebioda, Bojarska-Junak, Stanis?awowski, Cyman, Wierzbicki, Roli?ski, Celi?ski, Kmie?: TL1A as a potential local inducer of IL17A Expression in colon mucosa of inflammatory bowel disease patients. in Scandinavian journal of immunology 2015
TNFSF15 polymorphisms may contribute to genetic susceptibility of inflammatory bowel disease (Meta-Analysis)
TL1A modulated Rheumatoid arthritis-fibroblast-like synoviocytes migration and Indian hedgehog signaling pathway using TNFR2.
TL1A can induce tumor cell proliferation and promote the occurrence of colitis-associated colorectal cancer by activating Wnt/beta-catenin pathway.
TNFSF15, a cytokine mainly produced by blood endothelial cells, facilitates tumor lymphangiogenesis by upregulating VEGFC expression in A549 cells.
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) in renal cell carcinoma (RCC) cells in vitro. Overexpression of VEGI174, V7 or V8 inhibited EMT.
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)
play a role in the development of systemic sclerosis
the DR3/TL1A pathway directly enhances human OC formation and resorptive activity, controlling expression and activation of CCL3 and MMP-9.
the blocking of tumor necrosis factor receptor 2 (TNFR2) decreased TL1A-stimulated IL-6 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, -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) in renal cell carcinoma (RCC) in vivo. This may provide a new approach for the treatment of RCC
Data suggest that human regulatory T-lymphocytes express DR3 and demonstrate DR3/TL1A-mediated activation of signaling via MAP kinases and NFkappaB. (DR3 = death receptor 3; TL1A/TNFSF15 = tumor necrosis factor [ligand] superfamily, member 15)
These results raise the possibility for involvement of TL1A/DR3/DR3-mediated mechanisms in epithelial-mesenchymal interactions and the development of inflammation-induced intestinal fibrosis in Crohn's disease.
rs1250569 (ZMIZ1) and rs10114470 (TL1A) are two novel loci that indicate susceptibility to Inflammatory Bowel Disease in Han-Chinese patients.
results support an idea that the genetic susceptibility of TNFSF15 to CD may be confounded, in part, by the increase of Prevotella
(188)Re-NGR-VEGI has the potential as a theranostic agent.
miRNA-31 can directly bind to the 3-UTR of TNFSF15, thereafter negatively regulating its expression in Caco2 cells.
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)