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The TNFRSF1A c.625+10 G allele was associated with late response to anti-TNFalpha (zeige TNF Proteine) therapy but TNFRSF1A gene SNPs is not associated with spondyloarthritis.
TNFR1 is associated longitudinally with kidney function decline but not with myocardial infarct, heart failure, or mortality risk after adjustment
One third of our childhood MS patients had a heterozygous mutation in the TNFRSF1A and/or MEFV (zeige MEFV Proteine) gene. This proportion by far exceeds the number of mutations expected and was higher than in adult MS patients, suggesting that these mutations might contribute to the pathogenesis of childhood MS.
Studied the association of NLR family pyrin domain containing 3 (NLRP3 (zeige NLRP3 Proteine)) and tumor necrosis factor receptor superfamily member 1A (TNFRSF1A) polymorphisms and haplotypes in patients with ankylosing spondylitis (AS) and treatment response to etanercept.
Investigations of underlying molecular mechanisms of TNFR1 signaling showed that PDF affects TNFR1 signaling at the proapoptotic signaling pathway by upregulation of IkappaBalpha (zeige NFKBIA Proteine) and downregulation of cFLIPL.
Case Report: tumor necrosis factor (zeige TNF Proteine) receptor-associated periodic syndrome due to the R92Q TNFRSF1A variant associated with recurrent pericarditis and cardiac tamponade.
Serum TNFR1 is a biomarker for patients with chronic kidney disease.
This study demonstrated that TNFR1 expression levels are related to major depressive disorder and conjunctly mediate the effect of childhood maltreatment history on the risk of developing major depressive disorder.
Data suggest that Fas (zeige FAS Proteine) and TNFR1 are involved in glaucoma mechanisms in cornea; pro-apoptotic effect of anti-glaucoma medication clonidine on corneal epithelial cells triggers Fas (zeige FAS Proteine)/TNFR1-mediated, mitochondria-dependent signaling pathway. (Fas (zeige FAS Proteine) = Fas (zeige FAS Proteine) cell surface death receptor ; TNFR1 = TNF (zeige TNF Proteine) receptor superfamily member 1A)
These results indicate that TNFRI-Fc and hHO-1 overexpression may apparently induce free iron in the liver and exert oxidative stress by enhancing reactive oxygen species production and block normal postneonatal liver metabolism.
Results provide experimental data on the existence of a TNFRp55-mediated anti-inflammatory circuit in dendritic cells which might contribute to the protection against reactive arthritis during the resolution of Yersinia entercolitica infection.
TNFR1 contributes to ethanol-induced hypertension and oxidative stress in the vasculature.
TNFR2 (zeige TNFRSF1B Proteine) is important for the proliferative expansion of pathogenic Teff cells
NEMO (zeige IKBKG Proteine) deficiency hampered activation of IKK (zeige CHUK Proteine) complex in osteoclast precursors, causing arrest of osteoclastogenesis and apoptosis. Interestingly, inhibiting apoptosis by genetic ablation of TNFr1 significantly increased cell survival, but failed to rescue osteoclastogenesis or reverse osteopetrosis (zeige CSF1 Proteine).
Data indicate that IL-1RI and TNF (zeige TNF Proteine)-1R contribute to regulation of stress-induced, negatively reinforced drinking perhaps through overlapping signaling events downstream of these receptors, while leaving rewarding properties of alcohol largely unaffected.
Myeloid-derived suppressor cells from tumor necrosis factor (zeige TNF Proteine) receptor (TNFR) 2(-/-) mice, but not from TNFR1(-/-) mice, failed to promote B-cell responses.
TNFR2 (zeige TNFRSF1B Proteine) is required for inflammation-inducible M cells.
These findings indicate that TNFR1 is structurally positioned to modulate postsynaptic signaling in the PVN, suggesting a mechanism whereby TNFR1 activation contributes to cardiovascular and other autonomic functions.
Increased TNFR1 expression and signaling in injured peripheral nerves of mice with reduced BACE1 (zeige BACE Proteine) activity
Results show that interleukin 6 (IL6 (zeige IL6 Proteine)) promotes oval cell proliferation and liver regeneration, while tumor necrosis factor alpha (TNFalpha (zeige TNF Proteine)) and TNF (zeige TNF Proteine) receptor-1(TNFR1) do not affect this process.
Retinal ischemia results in increased expression of TNF-alpha (zeige TNF Proteine) and its receptors (TNF-R1 and TNF-R2 (zeige TNFRSF1B Proteine)).
Targeted gene knockdown of TNFRSF1B (zeige TNFRSF1B Proteine) in zebrafish embryos results in the induction of a caspase-8 (zeige CASP8 Proteine), caspase-2 (zeige CASP2 Proteine) and P53 (zeige TP53 Proteine)-dependent apoptotic program in endothelial cells that bypasses caspase-3 (zeige CASP3 Proteine).
These results suggest that TNF-alpha (zeige TNF Proteine) sources include immune cells, as well as large and small luteal cells, and that TNF-RI and TNF-RII (zeige TNFRSF1B Proteine) are present in the luteal cells of the bovine corpus luteum.
The expression and cellular localization of tumor necrosis factor-alpha (TNF (zeige TNF Proteine)) and its receptors (TNFRI and TNFRII (zeige TNFRSF1B Proteine)) mRNAs and proteins, were determined.
The upregulation of TNFRI mRNA expression by IFNG (zeige IFNG Proteine) suggests that TNF (zeige TNF Proteine) and IFNG (zeige IFNG Proteine) synergistically affect the death of luteal endothelial cells resulting in acute luteolysis
TNF (zeige TNF Proteine) binding induces release of AIP1 (DAB2IP (zeige DAB2IP Proteine)) from TNFR1, resulting in cytoplasmic translocation and concomitant formation of an intracellular signaling complex comprised of TRADD (zeige TRADD Proteine), RIP1 (zeige RALBP1 Proteine), TRAF2 (zeige TRAF2 Proteine), and AIPl.
The protein encoded by this gene is a member of the TNF-receptor superfamily. This protein is one of the major receptors for the tumor necrosis factor-alpha. This receptor can activate NF-kappaB, mediate apoptosis, and function as a regulator of inflammation. Antiapoptotic protein BCL2-associated athanogene 4 (BAG4/SODD) and adaptor proteins TRADD and TRAF2 have been shown to interact with this receptor, and thus play regulatory roles in the signal transduction mediated by the receptor. Germline mutations of the extracellular domains of this receptor were found to be associated with the autosomal dominant periodic fever syndrome. The impaired receptor clearance is thought to be a mechanism of the disease.
, tumor necrosis factor binding protein 1
, tumor necrosis factor receptor 1A isoform beta
, tumor necrosis factor receptor superfamily member 1A
, tumor necrosis factor receptor type 1
, tumor necrosis factor-alpha receptor
, TNF receptor alpha chain
, tumor necrosis factor receptor 1
, tumor necrosis factor receptor type I
, p55 TNF receptor
, tumor necrosis factor receptor p60
, TNF Receptor 1 (TR1)
, tumor necrosis factor type I
, tumor necrosis factor receptor superfamily, member 1A
, tumor necrosis factor receptor superfamily member 1A-like
, tumor necrosis factor (TNF superfamily, member 2)
, tumor necrosis factor alpha
, tumor necrosis factor ligand superfamily member 2
, tumour necrosis factor