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Gene Information
Gene symbol: TNFRSF1A
Gene name: tumor necrosis factor receptor superfamily, member 1A
HGNC ID: 11916
Synonyms: TNF-R, TNFAR, TNFR60, TNF-R-I, CD120a, TNF-R55
Related Genes
Related Sentences
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PMID |
Sentence |
| 1 |
12858016
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Induction of nitric oxide synthase (NOS) by soluble glucocorticoid induced tumor necrosis factor receptor (sGITR) is modulated by IFN-gamma in murine macrophage.
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| 2 |
12858016
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Earlier study showed that glucocorticoid induced tumor necrosis factor receptor (GITR), a new TNFR family, activated murine macrophages to express inducible nitric oxide synthase (iNOS) and to generate nitric oxide (NO).
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| 3 |
12858016
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A possible involvement of pro-inflammatory cytokines on NO production by GITR was investigated in vitro systems and signaling molecules contributing to sGITR-induced iNOS production are determined in Raw 264.7 cells, a murine macrophage cell line.
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| 4 |
12858016
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The result showed that the synergy was afforded by the combination of GITR with IFN-g in a dose-dependent manner but IFN-gamma alone was not able to induce NOS.
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| 5 |
12858016
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No effects were observed with TNF-alpha, IL-1beta, or IL-6 co-treated with GITR.
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| 6 |
12858016
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To determine signaling molecules contributing to sGITR-induced iNOS production, a specific inhibitor for signal pathway proteins tested showed that PDTC (NF-kappaB) and genistein (tyrosine kinase) inhibited NOS induction significantly, while sodium orthovanadate (tyrosine phosphatase) potentiated NOS expression.
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| 7 |
12858016
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These results suggest that activations of NF-kappaB were involved in induction of iNOS by GITR and IFN-gamma priming caused earlier and stronger NF-kappaB activation.
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| 8 |
18026101
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The LPS hypersensitivity phenotype is not suppressed by mutations in Myd88, Trif, Tnf, Tnfrsf1a, Ifnb, Ifng or Stat1, genes contributing to LPS responses, and results from an abnormality extrinsic to hematopoietic cells.
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| 9 |
21393251
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Expression of proinflammatory cytokines, including Tnfa, Il17a, and Ifng, was up-regulated, whereas expression of antimicrobial peptides was down-regulated in the colon of Traf2(-/-) mice.
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| 10 |
21393251
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Moreover, a number of IL-17-producing helper T cells were increased in the colonic lamina propria of Traf2(-/-) mice.
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| 11 |
21393251
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Finally, deletion of Tnfr1, but not Il17a, dramatically ameliorated colitis in Traf2(-/-) mice by preventing apoptosis of colonic epithelial cells, down-regulation of proinflammatory cytokines, and restoration of wild-type commensal bacteria.
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| 12 |
22052597
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A total of 10 single nucleotide polymorphisms distributed in 6 genes (TNFRSF1A, IL12A, IL12B, IFNG, IL4, and IL10) were genotyped in 214 high-responders [hepatitis B surface antibody (anti-HBs) ≥1,000 mIU/ml] and 107 low-responders (anti-HBs: 10-99 mIU/ml).
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| 13 |
22052597
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In addition, a significant gene-gene interaction was found: the frequency of the combined genotypes IL12A rs2243115 TT and IL12B rs17860508 CTCTAA/CTCTAA was significantly higher in the low-response group than in the high-response group (P = 0.008, odds ratio = 2.19, 95% confidence interval = 1.23-3.93).
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| 14 |
22052597
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These findings suggest that polymorphisms in the IL12A and IL12B genes might play an important role jointly in determining the response to hepatitis B vaccination.
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