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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.
Due to the fact that the mutation was not inherited from the parents, it was likely that R426L was a de novo and novel mutation in the TNFRSF1A gene, which can trigger TRAPS or TRAPS-like symptoms.
this study evaluated TNFR1 -609G/T polymorphisms association with RA susceptibility in a sample of Mexican patients. Our results suggest that the TNFR1 -609G/T polymorphisms are not associated with RA susceptibility in a sample of Mexican patients.
Polymorphisms in the TNFR1 gene may have an impact on the symptomatology of schizophrenia in men. rs4149577 and rs1860545 SNPs were associated with the intensity of the Positive and Negative Syndrome Scale (PANSS) excitement symptoms in men, which may contribute to the risk of violent behavior.
Polymorphism of Promoter Region of TNFRSF1A Gene is associated with Radiotherapy Induced Oral Mucositis in Head and Neck Cancer.
five single nucleotide polymorphisms in the TNFRSF1A gene are not associated with autoimmune thyroid diseases in the Chinese Han population, but rs4149570 shows a weak association with Hashimoto's thyroiditis after adjusting for gender and age.
Genotype rs767455 was associated with the susceptibility of ankylosing spondylitis(AS), G allele of rs767455 exhibited an association with the risk of developing AS. Only rs1061622 was significantly associated with long-term efficacy of etanercept. The results suggest that TNFRSF1A and TNFRSF1B (show TNFRSF1B Proteins) polymorphisms were associated with susceptibility, severity, and the long-term therapeutic efficacy of etanercept of AS patients.
RACK1 (show GNB2L1 Proteins) associates with MOAP-1 (show MOAP1 Proteins) via electrostatic associations similar to those observed between MOAP-1 (show MOAP1 Proteins)/RASSF1A (show RASSF1 Proteins) and MOAP-1 (show MOAP1 Proteins)/TNF-R1. These events illustrate the complex nature of MOAP-1 (show MOAP1 Proteins) regulation and characterizes the important role of the scaffolding protein, RACK1 (show GNB2L1 Proteins), in influencing MOAP-1 (show MOAP1 Proteins) biology.
serum level did not decrease significantly after tonsillectomy with steroid pulse therapy in IgA nephropathy
The TNFRSF1A c.625+10 G allele was associated with late response to anti-TNFalpha (show TNF Proteins) therapy but TNFRSF1A gene SNPs is not associated with spondyloarthritis.
Our work suggested that TNF-alpha (show TNF Proteins) and TNF-R1 are the major contributors of TNF (show TNF Proteins) signaling pathway in anesthesia-induced spinal cord neurotoxicity. Targeting TNF-alpha / TNF (show TNF Proteins)-R1, not TNF-R2 (show TNFRSF1B Proteins) signaling pathway may be the key component to rescue or prevent anesthesia-induced apoptotic injury in spinal cord neurons.
Lack of TNF-alpha (show TNF Proteins) 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 (show TNFRSF1B Proteins), is Required for Both Histaminergic and Non-histaminergic Itch in Mice.
p55TNFR shedding has a prominent role in Th1 (show HAND1 Proteins) mediated protection against chronic and latent tuberculosis infection
p55TNFR-IKK2 (show IKBKB Proteins)-Ripk3 (show RIPK3 Proteins) signalling orchestrates arthritogenic and death responses in synovial fibroblasts
his study shows that CCR-2 (show CCR2 Proteins)/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 (show TNFRSF1B Proteins) is important for the proliferative expansion of pathogenic Teff cells
NEMO (show IKBKG Proteins) deficiency hampered activation of IKK (show CHUK Proteins) 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 (show CSF1 Proteins).
Retinal ischemia results in increased expression of TNF-alpha (show TNF Proteins) and its receptors (TNF-R1 and TNF-R2 (show TNFRSF1B Proteins)).
Targeted gene knockdown of TNFRSF1B (show TNFRSF1B Proteins) in zebrafish embryos results in the induction of a caspase-8 (show CASP8 Proteins), caspase-2 (show CASP2 Proteins) and P53 (show TP53 Proteins)-dependent apoptotic program in endothelial cells that bypasses caspase-3 (show CASP3 Proteins).
These results suggest that TNF-alpha (show TNF Proteins) sources include immune cells, as well as large and small luteal cells, and that TNF-RI and TNF-RII (show TNFRSF1B Proteins) are present in the luteal cells of the bovine corpus luteum.
The expression and cellular localization of tumor necrosis factor-alpha (TNF (show TNF Proteins)) and its receptors (TNFRI and TNFRII (show TNFRSF1B Proteins)) mRNAs and proteins, were determined.
The upregulation of TNFRI mRNA expression by IFNG (show IFNG Proteins) suggests that TNF (show TNF Proteins) and IFNG (show IFNG Proteins) synergistically affect the death of luteal endothelial cells resulting in acute luteolysis
TNF (show TNF Proteins) binding induces release of AIP1 (DAB2IP (show DAB2IP Proteins)) from TNFR1, resulting in cytoplasmic translocation and concomitant formation of an intracellular signaling complex comprised of TRADD (show TRADD Proteins), RIP1 (show RALBP1 Proteins), TRAF2 (show TRAF2 Proteins), 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