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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.
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 polymorphisms were associated with susceptibility, severity, and the long-term therapeutic efficacy of etanercept of AS patients.
RACK1 associates with MOAP-1 via electrostatic associations similar to those observed between MOAP-1/RASSF1A and MOAP-1/TNF-R1. These events illustrate the complex nature of MOAP-1 regulation and characterizes the important role of the scaffolding protein, RACK1, in influencing MOAP-1 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 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 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) and tumor necrosis factor receptor superfamily member 1A (TNFRSF1A) polymorphisms and haplotypes in patients with ankylosing spondylitis (AS) and treatment response to etanercept.
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.
Data indicate that IL-1RI and TNF-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 receptor (TNFR) 2(-/-) mice, but not from TNFR1(-/-) mice, failed to promote B-cell responses.
TNFR2 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 activity
Results show that interleukin 6 (IL6) promotes oval cell proliferation and liver regeneration, while tumor necrosis factor alpha (TNFalpha) and TNF receptor-1(TNFR1) do not affect this process.
Data suggest that dietary treatment with green tea extract reduces hepatic inflammation in non-alcoholic fatty liver disease by decreasing proinflammatory signaling in liver through Tnfr1 (tumor necrosis factor receptor superfamily, member 1a) and Tlr4 (toll-like receptor 4) that otherwise increases NFkappaB activation and liver injury.
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