scholarly journals The chromosome 16q region associated with ankylosing spondylitis includes the candidate gene tumour necrosis factor receptor type 1-associated death domain (TRADD)

2009 ◽  
Vol 69 (6) ◽  
pp. 1243-1246 ◽  
Author(s):  
Jennifer J Pointon ◽  
David Harvey ◽  
Tugce Karaderi ◽  
Louise H Appleton ◽  
Claire Farrar ◽  
...  
Keyword(s):  
Ankylosing Spondylitis ◽  
Candidate Gene ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Receptor Type ◽  
Tumour Necrosis Factor Receptor ◽  
Death Domain ◽  
Meta Analyses ◽  
Necrosis Factor

ObjectiveTo replicate and refine the reported association of ankylosing spondylitis (AS) with two non-synonymous single nucleotide polymorphisms (nsSNPs) on chromosome 16q22.1.MethodsFirstly, 730 independent UK patients with AS were genotyped for rs9939768 and rs6979 and allele frequencies were compared with 2879 previously typed historic disease controls. Secondly, the two data sets were combined in meta-analyses. Finally, 5 tagging SNPs, located between rs9939768 and rs6979, were analysed in 1604 cases and 1020 controls.ResultsThe association of rs6979 with AS was replicated, p=0.03, OR=1.14 (95% CI 1.01 to 1.28), and a trend for association with rs9939768 detected, p=0.06, OR=1.25 (95% CI 0.99 to 1.57). Meta-analyses revealed association of both SNPs with AS, p=0.0008, OR=1.31 (95% CI 1.12 to 1.54) and p=0.0009, OR=1.15 (95% CI 1.06 to 1.23) for rs9939768 and rs6979, respectively. New associations with rs9033 and rs868213 (p=0.00002, OR=1.23 (95% CI 1.12 to 1.36) and p=0.00002 OR=1.45 (95% CI 1.22 to 1.72), respectively, were identified.ConclusionsThe region on chromosome 16 that has been replicated in the present work is interesting as the highly plausible candidate gene, tumour necrosis factor receptor type 1 (TNFR1)-associated death domain (TRADD), is located between rs9033 and rs868213. It will require additional work to identify the primary genetic association(s) with AS.

Effects of treatment on soluble tumour necrosis factor receptor type 1 and 2 in chronic periodontitis

2008 ◽  
Vol 35 (11) ◽  
pp. 961-968 ◽  
Author(s):  
Ikuyo Ikezawa-Suzuki ◽  
Yasuko Shimada ◽  
Hideaki Tai ◽  
Yasutaka Komatsu ◽  
Aya Tanaka ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Chronic Periodontitis ◽  
Tumour Necrosis ◽  
Receptor Type ◽  
Tumour Necrosis Factor Receptor ◽  
Necrosis Factor

scholarly journals Soluble tumour necrosis factor receptor type II and survival in colorectal cancer

2016 ◽  
Vol 114 (9) ◽  
pp. 995-1002 ◽  
Author(s):  
Ana Babic ◽  
Sonali M Shah ◽  
Mingyang Song ◽  
Kana Wu ◽  
Jeffrey A Meyerhardt ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Receptor Type ◽  
Tumour Necrosis Factor Receptor ◽  
Type Ii ◽  
Necrosis Factor

scholarly journals Endothelin-2 synthesis is stimulated by the type-1 tumour necrosis factor receptor and cAMP: comparison with endothelin-converting enzyme-1 expression

2000 ◽  
Vol 24 (2) ◽  
pp. 273-283 ◽  
Author(s):  
GL Lambert ◽  
S Barker ◽  
DM Lees ◽  
R Corder
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Receptor ◽  
Mrna Levels ◽  
Converting Enzyme ◽  
Dibutyryl Camp ◽  
Rt Pcr ◽  
Endothelin Converting Enzyme ◽  
Necrosis Factor

ABSTRACT The synthesis of the vasoconstrictor peptide endothelin-2 (ET-2) is dependent on hydrolysis of the biologically inactive intermediate big ET-2 by an endothelin-converting enzyme (ECE). Here, mechanisms inducing ET-2 synthesis have been investigated using the human renal adenocarcinoma cell line (ACHN). Synthesis of ET-2 by ACHN cells was inhibited by phosphoramidon (IC(50( congruent with11 microM). To determine whether ET-2 synthesis occurs in parallel with the metallopeptidase ECE-1, a putative processing peptidase for big ET-2, changes in the levels of their mRNAs were compared by semi-quantitative RT-PCR under conditions causing the upregulation of ET-2 synthesis. Tumour necrosis factor-alpha (TNFalpha), forskolin and a cell-permeable cAMP analogue (dibutyryl cAMP) caused concentration-dependent increases in ET-2 synthesis. Combination of forskolin or dibutyryl cAMP with TNFalpha produced a significantly greater increase in ET-2 production than these agents alone, indicating that adenylate cyclase and TNFalpha induce ET-2 synthesis by separate signalling pathways. Studies using receptor selective TNFalpha mutants, (125(I-TNFalpha binding and TNF receptor mRNA showed that type-1 TNF receptors mediate the ET-2 response to TNFalpha. PreproET-2 mRNA levels were increased by TNFalpha at 1 h and 2 h, but returned to control levels at 4 h. Treatment with forskolin significantly increased preproET-2 mRNA levels after 1 h and 4 h. ACHN cells expressed ECE-1b and ECE-1c, but not the ECE-1a isoform of this peptidase. RT-PCR for the combined isoforms ECE-1b/c/d showed TNFalpha to increase mRNA levels at 2 h and 4 h. Forskolin had no effect on ECE-1b/c/d mRNA levels. Thus, expression of ET-2 and ECE-1b/c/d mRNAs in ACHN cells do not display the co-ordinated regulation observed with typical peptide prohormone processing enzymes and their substrates.

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