Tumor necrosis factor receptor-associated periodic syndrome (TRAPS) is an autosomal dominant autoinflammatory condition caused by mutations in the TNFRSF1A gene which encodes the tumor necrosis factor (TNF) receptor, TNFR1.
Tumor necrosis factor receptor associated periodic syndrome (TRAPS) is an autosomic-dominant periodic syndrome associated with mutations in the extracellular domain of the 55 kDa TNF receptor.
TNF receptor-associated periodic fever syndrome (TRAPS) is an autosomal dominant systemic autoinflammatory disease caused by mutations of TNF receptor superfamily member 1 A (TNFRSF1A) gene.
This study suggests that SNPs at -308 and -857 of the TNFalpha promoter may represent an increased risk for the development of AVH but not for FHF in the Indian population.
TNF receptor-associated periodic syndrome (TRAPS) is a highly polymorphic autoinflammatory syndrome related to mutations in the TNFRSF1A gene encoding the type 1 TNF receptor.
Tumor necrosis factor receptor-associated periodic syndrome (TRAPS), formerly known as familial Hibernian fever, is the most common autosomal dominant autoinflammatory disease, resulting from mutations in the TNFRSF1A gene, encoding the 55-kD tumor necrosis factor receptor.
The diagnosis of periodic fever was made when molecular analysis revealed novel mutations in the tumor necrosis factor (TNF) receptor gene (TNFRSF1A), establishing the diagnosis of TNF receptor-associated periodic syndrome.
TRAPS is the first condition for which naturally occurring mutations in a TNF receptor were found; the mutations affect the soluble TNFRSF1A gene in the 12p13 region.
Tumour necrosis factor receptor-associated periodic syndrome (TRAPS) has been associated with several mutations in the TNF receptor super family 1A (TNFRSF1A), including most cysteine substitutions.
Canakinumab downregulated the TRAPS-causing gene (TNF super family receptor 1A (TNFRSF1A)), the drug-target gene (interleukin (IL)-1B) and other inflammation-related genes (eg, MAPK14).
Mutant tumor necrosis factor receptor associated with tumor necrosis factor receptor-associated periodic syndrome is altered antigenically and is retained within patients' leukocytes.
Tumor necrosis factor receptor-associated periodic syndrome is associated with mutations in the tumor necrosis factor receptor superfamily, member 1A (TNFRSF1A) gene which decreases the level of soluble tumor necrosis factor receptor-1 (TNFR1) leading to neutralization of tumor necrosis factor (TNF)-α.
Tumour necrosis factor receptor-associated periodic syndrome (TRAPS) results from point mutations in the extracellular domain of TNF receptor 1 (TNFRSF1A), but the effects of the mutations are controversial.
Role of tumour necrosis factor (TNF)-α and TNFRSF1A R92Q mutation in the pathogenesis of TNF receptor-associated periodic syndrome and multiple sclerosis.
This new concept includes a broad number of disorders, but the spotlight has been focused for the past two years on periodic fevers (familial Mediterranean fever [FMF]; mevalonate kinase deficiency [MVK]; tumor necrosis factor [TNF] receptor-associated periodic syndrome [TRAPS]; cryopyrin-associated periodic syndrome [CAPS]), Crohn's disease and Blau syndrome, thanks to the recent understanding of their molecular basis.
Tumor necrosis factor receptor-associated periodic syndrome (TRAPS) is an inherited autosomal-dominant autoinflammatory condition caused by mutations in the ectodomain of the 55-kd tumor necrosis factor (TNF) receptor superfamily 1A.
Their peripheral blood mononuclear cells (PBMC) had increased basal NF-kappaB activation compared with healthy controls and also had increased p50 nuclear expression following tumour necrosis factor (TNF) stimulation compared with PBMC from healthy controls, as well as T50M (T79M) and C88R (C117R) patients with TRAPS and patients with rheumatoid arthritis (RA).