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Validated All-in-One™ qPCR Primer for TNFRSF1A(NM_001065.3) Search again
Product ID:
HQP055535
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CD120a, FPF, TBP1, TNF-R, TNF-R-I, TNF-R55, TNFAR, TNFR1, TNFR55, TNFR60, p55, p55-R, p60
Gene Description:
TNF receptor superfamily member 1A
Target Gene Accession:
NM_001065.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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. [provided by RefSeq].
Gene References into function
- Despite the presence of functional TNFR2, TNFR1 associated with MAPK-dependent and -independent pathways is the primary signaling pathway involved in TNF alpha-induced synthetic functions in ASM cells.
- Here we report the expression and purification of the human TNF-RI DD as a fusion with the Escherichia coli thioredoxin A (TRX) protein
- induced marked apoptosis in T cells from HIV-infected persons; associated with both alteration of Bcl-2 expression and activation of caspase-8 and caspase-3
- insulin resistance and blood pressure are linked to altered shedding of TNF-alpha receptors in type 2 diabetes mellitus
- Autoimmune thyroid disease induced by thyroglobulin and lipopolysaccharide is inhibited by soluble TNF receptor type I.
- The human papillomavirus 16 E6 protein binds to tumor necrosis factor (TNF) R1 and protects cells from TNF-induced apoptosis
- Amino acid sequences located within an appropriately folded and functionally active death domain of the TNF receptor CD120a are both necessary and sufficient to promote the localization of the receptor to lipid rafts.
- Soluble TNF-alpha receptor I is an extracellular domain of TNFRI and antagonizes activities of TNF-alpha. Local transfection of the sTNFRI gene may have potential therapeutic value in vascular diseases in which TNF-alpha is also usually highly expressed.
- Altered signaling of TNFalpha-TNFR1 and SODD/BAG4 is responsible for radioresistance in human HT-R15 cells.
- mutation spectrum in genes in patients suffering from AA amyloidosis and recurrent inflammatory attacks
- Impaired glucose tolerance is not associated with increased serum concentrations.
- candidate genes that may be involved in the origination of ameloblastoma and several genes previously unidentified in relation to human tooth development.
- TNFRSF1A mutations were found in 28(7.1%) of 394 unrelated patients with tumor necrosis factor receptor-associated syndrome who have recurrent inflammatory syndromes.
- Review. p55TNFR is required for secondary lymphoid organ architecture & optimal antibody responses to T-dependent antigens. It has an enhancing role in antigen-specific T4 cell priming.
- Both adipose tissue and blood PAI-1 levels were positively associated with TNFRSF1A and TNFRSF1B in obesity.
- Increased sTNFRs-p55 levels in the serum and ascitic fluid reflect abnormal immune status of the patients with HCC and help predict the development of tumor.
- The role of TNF-R55 in the signaling pathway of neutral sphingomyelinase activation is enhanced by the interaction of RACK1 and FAN.
- Elevated serum levels of soluble TNF-alpha receptor type I are strongly associated with the development of acute renal failure in patients with septic shock.
- serum levels elevated in asthmatic patients during acute attack
- TNFR1 gene region might be a susceptible locus to type 1 diabetes in Japanese. Aberrant expresison or function of the receptor could be involved in the development of the disease.
- Polymorphism not associated with narcolepsy.
- Plasma sTNFR1 and sTNFR2 were inversely related to insulin sensitivity and might contribute to the development of insulin resistance in glucose-intolerant subjects.
- TNFR1 promoter polymorphisms are not associated with hereditary, familial, or idiopathic chronic pancreatitis
- plasma leptin levels, rather than nonesterified fatty acids and tumor necrosis factor receptor 1, may play a significant role in the development of hyperinsulinemia and insulin resistance in children
- TNFR1 apoptotic function is regulated by SODD/BAG4
- type 1 tumor necrosis factor receptor shedding aminopeptidase regulator(ARTS-1) promotes shedding of two cytokine receptor superfamilies, type I cytokine receptor superfamily (interleukin-6Ralpha) and tumor necrosis factor receptor superfamily (TNFR1)
- HCMV infection of fully permissive differentiated monocytic cell lines and U373 cells resulted in a reduction in cell surface expression of TNFRI and thus inhibition of TNFalpha signaling
- TNFR1 stimulates cytosolic phospholipase A2 (cPLA2) with distinct signaling mechanisms, by activating mitogen-activated protein kinase (MAPK) and p38MAPK, then phosphorylating and activating cPLA2 in a MAPK-dependent fashion.
- During leukocyte differentiation, time windows exist during which autocrine TNFalpha is active and then down-regulated by TNF receptor I, which may temper continuous up-regulation of synthesis of proteins involved in pericellular proteolysis.
- (-308) TNF-alpha gene polymorphism may contribute to CHD risk in patients with type 2 diabetes and can be useful predictive marker for the diagnosis of CHD in type 2 diabetic women.
- Missense mutations found in these genes are probably responsible for an improvement in function.
- Neither the +36 TNFRSF1A SNP nor the +196 TNFRSF1B SNP is associated with RA severity in a population of Caucasian patients with RA.
- High levels of the soluble, 55-kilodalton isoform of tumor necrosis factor receptor in bone marrow are correlated with the clinical outcome of children with acute lymphoblastic leukemia in first recurrence
- TNFR1 signals both cell survival and apoptosis.
- TNFR1-induced apoptosis involves two sequential signaling complexes.
- preferential induction of prodestructive and proinflammatory mediators in rheumatoid arthritis synovial fibroblasts by the TNF-R55
- genetic basis among patients with "TRAPS-like" features is heterogeneous and TNFRSF1A mutations are not commonly associated with nonfamilial recurrent fevers of unknown etiology.
- Tumour necrosis factor receptor-associated periodic syndrome (TRAPS) is a dominantly inherited disorder characterised by recurrent episodes of sustained fever.Here we report a case of TRAPS with a novel TNFRSF1A mutation, C70S, in a Japanese family.
- Epstein-Barr virus (EBV) immediate-early protein BZLF1 prevents TNF-alpha activation of target genes and TNF-alpha-induced cell death by down regulating TNF-R1
- carriers of the 92Q allele may be at increased risk of atherosclerosis
- The level of the sTNF-R1 was elevated in myelodysplastic syndrome(MDS) patients.
- Distribution of the TNFR2 196 R/R and TNFR1 +36 A/A genotypes in familial rheumatoid arthritis could suggest an interaction between TNFR1 and TNFR2 in the genetic susceptibility for rheumatoid arthritis.
- Expression of TNF-receptor 2 (TNF-R2) but not TNF-receptor 1 (TNF-R1) was detected in myeloma cell lines.
- relatively small number of genes may be involved in the clinical manifestation of hyperimmunoglobulinemia D, with low-penetrance TNFRSF1A variants possibly influencing the phenotype
- human tumour necrosis factor receptor 1 has a major region controlling cell surface expression
- Provided that TNF-R1 mediates the cytotoxic actions of TNFalpha, these results support the concept of dysregulated TNF alpha metabolism in alcoholic hepatitis.
- CpG islands are found within the promoter regions of both human and mouse TNFR1 (TNFRSF1) genes
- NAK is a component of the TNFalpha.TNFR1 signaling complex and has a physiological role in the TNFalpha-mediated response
- Two amino acid substitutions may be associated with chronic inflammatory disorders, such as SLE, or not.
- Although ischemic liver injury was not serious, due to the short ischemia time, TNFR1 and TRAIL are associated with liver ischemic injury in live-donor liver transplantation but Fas is not.
- activation of p38 MAPK and c-Jun N-terminal kinase pathways by hepatitis B virus X protein mediates apoptosis via induction of Fas/FasL and TNFR1/TNFa expression
- High frequency of TNFRSF1A polymorphism is associated with Sickle Cell Anemia
- TNFR1 signaling pathway via sphingomyelinase may play a role as an important regulator of T cell responses
- The C43S TNFRSF1A mutation results in decreased TNFalpha-induced nuclear signaling and apoptosis.
- Genetic variations in these proinflammatory mediators and their receptors appear to influence the susceptibility and severity of the inflammatory response within the eyes of patients during the development of IAU(idiopathic acute anterior uveitis).
- TNFR2 and TNFR1 signal transduction mechanisms involved in activation of NFkappaB and CMV promoter-enhancer were compared with respect to their susceptibility towards inhibitors of intracellular signaling.
- disabled TNFR1 function by inducing allosteric modulation of tryptophan-107 in the receptor. The allosteric effect operates by means of an allosteric cavity found a short distance from a previously identified loop involved in ligand binding.
- Patients with CRPS and mechanical hyperalgesia had higher levels of sTNF-RI compared with those with CRPS with identical clinical appearance but without hyperalgesia.
- phosphorylation of CREB is increased by 8-bromo-cAMP, which has opposite effects on TNF and TNFR1 mRNA expression
- Polymorphism within TNFRSF1A genes are associated with iron deficient anemia in patient diagnosed with rheumatoid arthritis.
- TNFR1 and TNFR2 have roles in cell type-specific renal injury
- This review presents the tumor necrosis factor receptor (TNFR)-associated periodic syndrome (TRAPS) as an autosomal dominant, multisystemic, autoinflammatory disorder caused by mutations in the TNFR1 gene (TNFRSF1A)
- PAK4 has a role in TNF-alpha induced cell survival pathyways by facilitating TRADD binding to the TNF Receptor
- TAK1 is recruited to the TNF-R1 complex via RIP and likely cooperates with MEKK3 to activate NF-kappaB in TNF-alpha signaling
- TNF-receptor-associated periodic syndrome is caused by mutations in the gene encoding TNFRSF1A on chromosome 12p13. (Review)
- TNFRSF1A is a modulation in Cystic Fibrosis.
- APN/CD13 regulates TNFalpha-induced apoptosis via inhibition of TNFRI shedding
- tumor necrosis factor alpha and TNFR1 and TNFR2 have roles in cellular differentiation
- inversely related to endothelium-dependent vaodilation in glucose intolerance.
- Abundant tumor necrosis factor receptor 1 (mTNFR1) expression was observed in the cytotrophoblast cells and chorionic villus stromal cells in women with spontaneous abortion.
- These findings suggest that EMAP-II sensitises endothelial cells to apoptosis by facilitating TNF-R1 apoptotic signalling via TRADD mobilization.
- Serum levels of soluble TNFRSF1A, measured along with the C-reactive protein level, may be a useful screening marker for differentiating tumor necrosis factor receptor-associated periodic syndrome from systemic juvenile idiopathic arthritis.
- These results suggest that genetic variations in the TNF-alpha gene and its receptor genes may not be involved in individual vulnerability to METH dependence.
- association between TNFRSF1A +36G/G genotype and the MetS renders obese women more prone to activation of the TNF pathway reflected by high circulating sTNFR1 and PAI-1 levels.
- TNFRSF1A investigation in rheumatoid arthritis from the French Caucasian population showed only the R92Q mutation, with a frequency of 4.5%, but no evidence for linkage to the disease
- TNF-RI and -RII promoter gene polymorphisms and variations in protein and gene expression of these receptors are unlikely to play a major role in the development of Alzheimer's disease
- TNFR-1 mediated apoptosis is stimulated by a dominant negative functional domain on DAPK-1
- analyzed candidate genes related to TNFalpha regulation and found that interleukin (IL)-10, interferon-gamma receptor 1 (IFNGR1), and TNFalpha receptor 1 (TNFR1) genes were linked and associated to both tuberculosis and TNFalpha
- Periodic fever syndrome is associated with Tumor necrosis factor receptor-1A mutation C30R (cysteine to arginine) in a Japanese family.
- TNFRSF1A with the C33Y mutation has an abnormal structure in leukocytes of patients with TNFR-associated periodic syndrome.
- The result suggests that pregnancy failure is associated with an increase of soluble TNFR1.
- No increase in TNF receptor I gene or protein expression was observed in degenerate or herniated intervertebral discs.
- odds ratios obtained (0.64 for multiple sclerosis and 0.91 for Wegener's granulomatosis ) do not indicate a significant association of the R92Q allele with these diseases
- association between persistent palindromic rheumatism and SNPs within the TNFRSF1A gene.
- Transmembrane tumor necrosis factor (TNF) and TNF receptor (TNFR)1/2 are interaction partners contributing to TNF-alpha production in monocytes.
- Value of serum TNFR1 concentration as a marker of response to phototherapy may depend on duration of skin lesions and the treatment method.
- As TNF-R1 is increased in substantia nigra of Parkinsonian brains, nonvesiculated DA might also play a role in inducing TNF-R1 expression and predispose the neuron to the action of cytokines released in a microglia-mediated inflammatory response.
- Downregulation of survivin causes changes in mitosis and apoptosis, which may be related to changes in TNF receptors and NF-kappaB signaling.
- Data show that Type D personality is associated with substantially increased TNFR1 and TNF-alpha activity.
- Thus, a distinct population of TNFR1 exosome-like vesicles circulate in human plasma and may modulate TNF-mediated inflammation.
- The increase of plasma TNF-alpha in amyotrophic lateral sclerosis (ALS) patients in the presence of a slight increase of sTNFR-1 & -2 supports a functionally significant activation of the TNF system in ALS.
- A novel, TRAPS causing, TNFRSF1A splice site mutation is associated with decreased sTNFR1 levels, cell surface and whole cell extract expression and increased NF-kappaB transcription factor activation
- High levels of TNFRI at the cell surface in patients with the C73R mutation hypersensitizes cells to stimulation by TNF, leading to increased NF-kappaB p65 subunit activation and an exaggerated proinflammatory response
- TNFR1 accumulated at the chlamydial inclusion and was shed by the infected cell into the culture supernatant. Receptor shedding depended on the infection-induced activation of the MEK-ERK pathway and the metalloproteinase TACE
- TNFRSF1A sequencing disclosed a novel V173D/p.Val202Asp substitution encoded by exon 6 in one family, the c.194-14G>A splice variant in another and the R92Q/p.Arg121Gln substitution in two families.
- TNF-alpha-308 G/A may be related to susceptibility, whereas -609 TT TNFR1 and 1690 C/T TNFR2 SNPs may be protective to tobacco-related oral squamous cell carcinoma.
- Therefore, our results suggest that TNFR1 -329G/T polymorphism may play an important role in the development of HCC.
- These results suggest that tumour necrosis factor receptor genotypes may be involved in the different responses to infliximab in Japanese patients with Crohn's disease.
- amniotic fluid sTNF-R1 levels did not differ significantly before and after labor
- Wer report a TNFRSF1A R92Q mutation in association with a multiple sclerosis-like demyelinating syndrome.
- In patients with heart failure, increased sTNFR-1 as an expression of chronic inflammation is correlated with both anemia and low serum lipid fractions.
- The circulating levels of sTNF-R1 increased in non-transmitting and transmitting mothers and in Trypanosoma cruzi-infected and non-infected neonates.
- Our findings also suggest that polymorphisms at IL23R and TNFRSF1A, and possibly HLA and TLR4, loci may account for phenotypic variation in IBD.
- Report expands the spectrum of TNFRSF1A mutations associated with TRAPS, adding further evidence for possible additive effects of a low-penetration R92Q and cysteine residue mutations, and confirms etanercept as an efficacious treatment alternative.
- sTNFR1 and sTNFR2 were found at increased plasma concentrations in active Behcet's disease (BD), with the highest concentration in active BD with arthritis.
- This identifies RBMX as an ARTS-1-associated protein that regulates both the constitutive release of TNFR1 exosome-like vesicles and the inducible proteolytic cleavage of TNFR1 ectodomains.
- Higher percentage of peritoneal fluid macrophages expressing TNFR1 and TNFR2 proteins in endometriosis suggests dependence of these cells on TNF-alpha stimulation.
- Increases in TNFR1( tumor necrosis factor receptor type 1) level at day 7 post allogeneic hematopoietic cell transplant correlated with the severity of GVHD and survival in pediatric patients
- oxidative stress promotes TNFR receptor (TNFR1- and TNFR2) self-interaction and ligand-independent and enhanced ligand-dependent TNF signaling
- data showed that TNFRI polymorphisms have an important role in auimmune thyroid disease pathogenesis in both familial and case-control samples
- study shows that TNFR1 associates with Jak2, c-Src, and PI3K in various cell types to engage signaling pathways, activate transcription factors, and modulate gene expression
- both the constitutive and cAMP-induced release of TNFR1 exosome-like vesicles occur via PKA-dependent pathways that are regulated by the anchoring of RIIbeta to BIG2 via AKAP domains B and C
- Serum levels of sTNFR1 and sTNFR2 were increased in schizophrenic patients when compared with controls (all p < 0.05), but there was no difference in TNF-alpha levels.
- An upregulated TNFR2-dependent plays a role in acute-phase motor axonal neuropathy.
- amniotic fluid TNF-alpha and soluble TNF receptor concentration regulation is affected by race and preterm birth
- Alix and ALG-2 are new actors of the TNF-R1 pathway
- In most cases with MS and coexisting TRAPS, features of MS were quite typical, whereas TRAPS presented mostly without the fever episodes observed in childhood. The penetrance of the R92Q mutation in affected family members was higher than reported.
- The results suggested that R31A and R32G mutations strongly influenced electrostatic interaction with TNFR2, and that L29K mutation contributed to the binding of R1-6 to TNFR1.
- periodic syndrome-associated TNFRI mutants induce the expression of multiple genes encoding inflammatory molecules, cellular receptors, transcription factors, and regulators of apoptosis in endothelial cells