The −308 tumor necrosis factor-α promoter polymorphism effects transcription

Kroeger, Karen M.; Carville, Keryln; Abraham, Lawrence J.

doi:10.1016/s0161-5890(97)00052-7

Cited by 820 publications

(573 citation statements)

References 25 publications

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“…However, the South Croatian families analyzed in this study have not been HLA typed and therefore we can not determine whether the effects of the TNF/LTA variants are primary or secondary to HLA loci. A functional support for independent effects may be explained by transcription rate enhancement of TNF gene by TNF promoter −308 and −238 SNPs, functional control of TNF promoter SNPs on LTA expression and expression of other nearby genes [34,35,[37][38][39]. An integrated role of TNF and other inflammatory cytokines in the destruction of pancreatic beta cells [19] provides further argument for a TNF/LTA T1DM effect.…”

Section: Discussionmentioning

confidence: 95%

“…Interestingly, overtransmission of A-G rs1800629(G-308A)-rs361525(G-238A) haplotype shows stronger significance (2.384×10 −5 ) than any of the single markers individually (rs1800629 (G-308A), p = 1.2×10 4 ; rs361525(G-238A), p = 8.15×0 −3 ). As both promoter polymorphisms have been associated with transcriptional enhancement rate it is possible that when acting in cis these two markers show an even stronger interaction [33][34][35].…”

Section: Discussionmentioning

confidence: 99%

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Family-based analysis of tumor necrosis factor and lymphotoxin-α tag polymorphisms with type 1 diabetes in the population of South Croatia

et al. 2009

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Family-based analysis of tumor necrosis factor and lymphotoxin-α tag polymorphisms with type 1 diabetes in the population of South Croatia

et al. 2009

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“…[189][190][191] Wilson et al were also unable to provide evidence of a major difference in affinity of DNA binding proteins in this study. Another group has published several studies 192,193 using À308 constructs and were unable to detect a difference in the activity of variants lacking the 3 0 UTR in contrast to Wilson et al, but did observe differences when the 3 0 UTR was present, in contrast to the study of Brinkman et al…”

Section: Ex Vivo Tnf Productionmentioning

confidence: 87%

Is there a future for TNF promoter polymorphisms?

2004

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The in vitro study of TNF promoter polymorphism (SNP) function was stimulated by the numerous case-control (association) studies of the polymorphisms in relation to human disease and the appearance of several studies claiming to show a functional role for these SNPs provided a further impetus to researchers interested in the role of TNF in their disease of interest. In this review we consider case-control studies, concentrating on the autoimmune and inflammatory diseases rheumatoid arthritis, multiple sclerosis, ankylosing spondylitis, and asthma, and on infectious diseases including malaria, hepatitis B and C infection, leprosy and sepsis/septic shock. We also review the available evidence on the functional role of the various TNF promoter polymorphisms. In general, case-control studies have produced mixed results, with little consensus in most cases on whether any TNF polymorphisms are actually associated with disease, although results have been more consistent in the case of infectious diseases, particularly malaria. Functional studies have also produced mixed results but recent work suggests that the much studied À308G/A polymorphism is not functional, while the function of other TNF polymorphisms remains controversial. Studies of the TNF region are increasingly using extended haplotypes that can better capture the variation of the MHC region.

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“…Increased progression was seen when the data were analyzed using the continuous variable (i.e., weighted or unweighted radiographic progression rates per year), when radiographic change was classified as progressive or not progressive (50), and when baseline characteristics were adjusted using multiple logistic regression. This association may be due to higher production of TNF␣ associated with the -308 G-to-A polymorphism (28,31). For example, in a juvenile idiopathic arthritis cohort from Turkey, the -308 G-to-A polymorphism was associated with a poor clinical course (56).…”

Section: Discussionmentioning

confidence: 99%

“…Many investigators have found that the A allele of the TNFA -308 polymorphism may influence transcriptional activity, with the downstream effect of increased production of TNF␣ (28,(31)(32)(33)(34)(35). However, other investigators have not found any functional significance of the -308 G-to-A substitution (36)(37)(38).…”

mentioning

confidence: 99%

Association of tumor necrosis factor α polymorphism, but not the shared epitope, with increased radiographic progression in a seropositive rheumatoid arthritis inception cohort

Khanna

Park

et al. 2006

Arthritis & Rheumatism

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Objective. To determine whether the tumor necrosis factor ␣ (TNFA) -308 guanine-to-adenosine polymorphism and/or the shared epitope (SE) is associated with radiographic damage in patients with early rheumatoid arthritis (RA).Methods. The cohort consisted of 189 patients with early seropositive RA (median 5.6 months since symptom onset) who had active disease, no previous disease-modifying antirheumatic drug treatment, and >2 sets of scored radiographs of the hands/wrists and forefeet. TNFA -308 polymorphism was analyzed by polymerase chain reaction pyrosequencing. The SE was defined as presence of any 1 of the following HLA-DRB1 alleles: *0101, *0102, *0401, *0404, *0405, *0408, *0410, *1001, *1402, or *1406. Radiographic progression was assessed by the total Sharp score.Results. Using a weighted least-squares regression analysis, patients with the -308 TNFA AA plus AG genotypes (n ‫؍‬ 49) had significantly higher rates of progression in erosion scores (median 0.84 versus 0.48 units/year), joint space narrowing (JSN) scores (0.42 versus 0.04), and total Sharp scores (1.70 versus 0.61) compared with patients with the TNFA GG genotype (n ‫؍‬ 140). Presence of the SE (n ‫؍‬ 137) was associated with significantly lower progression rates (per year) for total Sharp scores (median 0.9 versus 1.25 units/year) and JSN scores (0.04 versus 0.41), but not for erosion scores (0.50 versus 0.61) compared with patients without the SE (n ‫؍‬ 52). In a least-squares multiple linear regression model, the presence of the AA plus AG genotypes was associated with a significantly higher progression rate after adjusting for the presence of the SE, interaction between the SE and the AA plus AG genotypes, baseline log C-reactive protein level, Health Assessment Questionnaire Disability Index, total Sharp score, swollen joint count, and presence of osteophytes (osteoarthritis). There was a strong linkage disequili-

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The −308 tumor necrosis factor-α promoter polymorphism effects transcription

Cited by 820 publications

References 25 publications

Family-based analysis of tumor necrosis factor and lymphotoxin-α tag polymorphisms with type 1 diabetes in the population of South Croatia

Family-based analysis of tumor necrosis factor and lymphotoxin-α tag polymorphisms with type 1 diabetes in the population of South Croatia

Is there a future for TNF promoter polymorphisms?

Association of tumor necrosis factor α polymorphism, but not the shared epitope, with increased radiographic progression in a seropositive rheumatoid arthritis inception cohort

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