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This study did not find an association between TNFRSF1A multiple sclerosis-associated single nucleotide polymorphisms and the occurrence of demyelination events related to TNFalpha inhibitors
Increase in serum sTNFR II level and elevated sTNFR II/I ratio may be promising indicators of the development of coronary artery lesions in Kawasaki disease.
This preliminary study shows a significant association between higher sTNFRI and lower scores on the short-term visual memory delayed match to sample test in breast cancer patients receiving chemotherapy
In the in vitro model, exposing Caco-2 cells to tumor necrosis factor-alpha (TNF-alpha) led to a significant inhibition in RF uptake, an effect that was abrogated upon knocking down TNF receptor 1 (TNFR1). The inhibition in RF uptake was associated with a significant reduction in the expression of hRFVT-3 and -1 protein and mRNA levels, as well as in the activity of the SLC52A3 and SLC52A1 promoters
From these experiments, we gained no evidence for inhibitory effects of high concentrations (20-500 nM) of PGRN on the interaction of TNF with TNFR1 and TNFR2.
It can be concluded that the mRNA levels of TNFR1 and TNFR2 were not associated with coronary artery disease risk
increased circulating levels of sTNFR1 and BNP were associated with loss of kidney function in Type 2 diabetic Egyptian patients
Specificity of human anti-variable heavy (VH ) chain autoantibodies and impact on the design and clinical testing of a VH domain antibody antagonist of tumour necrosis factor-alpha receptor 1.
TNF receptor 1 (TNFR1)-induced necroptosis is known to require the formation of a RIPK1-RIPK3-mixed lineage kinase domain-like pseudokinase (MLKL) signaling complex (necrosome) that we find compartmentalizes exclusively to caveolin-1-associated detergent-resistant membrane (DRM) vesicles in HT-29 cells.
rs1900693 is not associated with the severity of ankylosing spondylitis and responses to anti-tumour necrosis factor biologics.
Staphylococcus aureus protein A enhances osteoclastogenesis via TNFR1 and EGFR signaling
In rare cases, periodic fever and inflammatory symptoms in adults can be attributed to mutations in NLRP3, MVK and TNFRSF1A.
Using a small amount of peripheral blood, successfully detected possible neuron-derived exosome-related blood biomarkers. This is the first study to suggest that not only SYP and TNFR1 but also IL34 are important blood biomarkers for patients with Manic Depressive Disorder.
The soluble TNF-RII/I ratio increased profoundly as macrophage activation syndrome developed and correlated positively with disease activity
Serum TNFR1 concentrations are associated with major amputation in patients with type 2 diabetic patients.
Here, we reported a new PET tracer for targeting TNFR1.
TNFRSF1A is a STAT3 target gene that regulates the NF-kappaB pathway.
by restraining TNFR1 at the cell surface via sialylation, ST6Gal-I acts as a functional switch to divert signaling toward survival. These collective findings point to a novel glycosylation-dependent mechanism that regulates the cellular response to TNF and may promote cancer cell survival within TNF-rich tumor microenvironments.
Elevated TNFRs levels were associated with the risk of cardiovascular and/or all-cause mortality independent of all relevant covariates in patients undergoing haemodialysis
It has been demonstrated that the molecular genetic marker +36G TNFR1 (OR=1,25) is involved in the formation Essential Hypertension in individuals with Metabolic Syndrome.
Taken together these results indicate that TNFR1 plays a critical role on T cell dysfunction during Staphylococcus aureus sepsis by regulating immunomodulatory mediators in myeloid derived suppressor cells.
TNF-alpha-TNF-Rp55 axis may have essential roles in the resolution of venous thrombus in mice.
we conclude that signal integration by NF-kappaB protects developing natural killer T (NKT) cells from death signals emanating from TNFR1, but not from the NKT TCR or Fas.
The results of this study suggest that TNFR1 signaling plays an essential role in pain induction after CCI in males but not in females
In conclusion, these data provide evidence for a regulatory role of TNF-alpha in diesel exhaust particles-induced pulmonary inflammation and identify TNFR2 as the most important receptor in mediating these inflammatory effects.
Atherosclerotic pathology in each Chlamydia pneumoniae (CPN)-infected knockout (KO)mouse group was reduced significantly compared to WT mice, suggesting that both TNFR1 and TNFR2 promote CPN-induced atherosclerosis.
TNF, via TNFRp55 signaling, modulates articular progesterone and cytokine circadian rhythms in late pregnancy.
Recognition memory improved with exercise in WT mice, was impaired in TNFR1(-/-) exercise mice, showed non-significant impairment with exercise in TNF(-/-) mice, and no changes in TNFR2(-/-) mice. In spatial learning there were exercise related improvements in WT mice, non-significant but meaningful impairments evident in TNFR1(-/-) exercise mice, modest improvement in TNF(-/-) exercise mice.
Transmembrane TNF, TNFR2 and TNFR1 (indirectly) are critical for preventing inflammation during BCG-induced pleurisy in mice.
Our work suggested that TNF-alpha and TNF-R1 are the major contributors of TNF signaling pathway in anesthesia-induced spinal cord neurotoxicity. Targeting TNF-alpha / TNF-R1, not TNF-R2 signaling pathway may be the key component to rescue or prevent anesthesia-induced apoptotic injury in spinal cord neurons.
Lack of TNF-alpha signaling through Tnfr1 makes the mice more susceptible to acute infection but does not alter state of latency and reactivation of HSV-1.
This study demonstrated that the TNFR1, but not TNFR2, is Required for Both Histaminergic and Non-histaminergic Itch in Mice.
p55TNFR shedding has a prominent role in Th1 mediated protection against chronic and latent tuberculosis infection
p55TNFR-IKK2-Ripk3 signalling orchestrates arthritogenic and death responses in synovial fibroblasts
his study shows that CCR-2/TLR-2 triggered signaling in murine peritoneal macrophages intensifies bacterial (Staphylococcus aureus) killing by reactive oxygen species through TNF-R1
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 is important for the proliferative expansion of pathogenic Teff cells
NEMO deficiency hampered activation of IKK 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.
Results indicated that TNFRSF1A activated the TNF signaling pathway and inhibited the NFkappaB signaling pathway in vitro. These findings provide evidence for an immune-related regulatory function for porcine TNFRSF1A.
Retinal ischemia results in increased expression of TNF-alpha and its receptors (TNF-R1 and TNF-R2).
Targeted gene knockdown of TNFRSF1B in zebrafish embryos results in the induction of a caspase-8, caspase-2 and P53-dependent apoptotic program in endothelial cells that bypasses caspase-3.
These results suggest that TNF-alpha sources include immune cells, as well as large and small luteal cells, and that TNF-RI and TNF-RII are present in the luteal cells of the bovine corpus luteum.
The expression and cellular localization of tumor necrosis factor-alpha (TNF) and its receptors (TNFRI and TNFRII) mRNAs and proteins, were determined.
The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of luteal endothelial cells resulting in acute luteolysis
TNF binding induces release of AIP1 (DAB2IP) from TNFR1, resulting in cytoplasmic translocation and concomitant formation of an intracellular signaling complex comprised of TRADD, RIP1, TRAF2, 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