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anti-Human TNFRSF1B Antikörper:
anti-Mouse (Murine) TNFRSF1B Antikörper:
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Human Monoclonal TNFRSF1B Primary Antibody für FACS - ABIN4897938
Saito, Hirokawa, Inaba, Fukaya, Kawabata, Komatsuda, Yamashita, Sawada: Phagocytosis of codeveloping megakaryocytic progenitors by dendritic cells in culture with thrombopoietin and tumor necrosis factor-alpha and its possible role in hemophagocytic syndrome. in Blood 2006
Show all 11 Pubmed References
Human Monoclonal TNFRSF1B Primary Antibody für FACS - ABIN2688926
Gehr, Gentz, Brockhaus, Loetscher, Lesslauer: Both tumor necrosis factor receptor types mediate proliferative signals in human mononuclear cell activation. in Journal of immunology (Baltimore, Md. : 1950) 1992
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Human Monoclonal TNFRSF1B Primary Antibody für FACS, ELISA - ABIN2688927
Aggarwal, Gollapudi, Gupta: Increased TNF-alpha-induced apoptosis in lymphocytes from aged humans: changes in TNF-alpha receptor expression and activation of caspases. in Journal of immunology (Baltimore, Md. : 1950) 1999
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Mouse (Murine) Polyclonal TNFRSF1B Primary Antibody für CyTOF, FACS - ABIN4899742
Williams, Mistry, Guillard, Ulrichsen, Sandercock, Wang, González-Muñoz, Parmentier, Black, Soden, Freeth, Jovanović, Leyland, Al-Lamki, Leishman, Rust, Stewart, Jermutus, Bradley, Bedian et al.: Phenotypic screening reveals TNFR2 as a promising target for cancer immunotherapy. ... in Oncotarget 2016
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Human Monoclonal TNFRSF1B Primary Antibody für CyTOF, FACS - ABIN4900548
Georgopoulos, Steele, Thomson, Selby, Southgate, Trejdosiewicz: A novel mechanism of CD40-induced apoptosis of carcinoma cells involving TRAF3 and JNK/AP-1 activation. in Cell death and differentiation 2006
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Human Monoclonal TNFRSF1B Primary Antibody für FACS - ABIN4897936
Tufa, Chatterjee, Low, Schmidt, Jacobs: TNFR2 and IL-12 coactivation enables slanDCs to support NK-cell function via membrane-bound TNF-α. in European journal of immunology 2014
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Mouse (Murine) Monoclonal TNFRSF1B Primary Antibody für CyTOF, ELISA (Capture) - ABIN4900547
Osuchowski, Welch, Siddiqui, Remick: Circulating cytokine/inhibitor profiles reshape the understanding of the SIRS/CARS continuum in sepsis and predict mortality. in Journal of immunology (Baltimore, Md. : 1950) 2006
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Mouse (Murine) Polyclonal TNFRSF1B Primary Antibody für Func, IA - ABIN2192162
Lucas, Garcia, Donati, Hribar, Mandriota, Giroud, Buurman, Fransen, Suter, Nunez, Pepper, Grau: Both TNF receptors are required for direct TNF-mediated cytotoxicity in microvascular endothelial cells. in European journal of immunology 1998
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Mouse (Murine) Monoclonal TNFRSF1B Primary Antibody für Func, IA - ABIN2191752
Tacchini-Cottier, Vesin, Redard, Buurman, Piguet: Role of TNFR1 and TNFR2 in TNF-induced platelet consumption in mice. in Journal of immunology (Baltimore, Md. : 1950) 1998
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Mouse (Murine) Monoclonal TNFRSF1B Primary Antibody für Func, IA - ABIN2191751
Brekke, Sagen, Bjerve: Specificity of endogenous fatty acid release during tumor necrosis factor-induced apoptosis in WEHI 164 fibrosarcoma cells. in Journal of lipid research 2000
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Results suggests that the TNFR2 rs1061624 polymorphism is associated with hepatitis B virus-related chronic hepatitis B, liver cirrhosis, and hepatocellular carcinoma in Chinese population, particularly in males.
The combinational effects of rs1061622 and rs1061624 in TNFRSF1B gene may increase the risk of hepatitis C chronicity and infection.
The authors identified two potentially functional single nucleotide polymorphisms (IKBKAP rs4978754 C > T and TNFRSF1B rs677844 T > C) to be associated with survival of patients with non-small cell lung cancer.
Study finds that in primary human T regulatory cells (T-regs) TNFR2 ligation initially uses canonical NF-kappaB signaling to prime and then activate non-canonical NF-kappaB signaling and that the latter pathway enhances the proliferative response of T-regs to IL2.
There is an association between circulating sTNFR1 and sTNFR2 and risk of myocardial infarction that is different for Swedish males and females
Increased concentrations of circulating TNFR1 and TNFR2 were associated with increased risks of cardiovascular events and mortality in patients with stable coronary heart disease.
our data provides a novel insight about the complex interplay between Th17 and Treg subsets in which Th17 cells potentially stimulate the increased frequency of Tregs. This effect is mainly mediated by TNF-alpha-TNFR2 signaling pathway.
TNFR2 diverts the tumor-inhibiting TNF into a tumor-advocating factor. TNFR2 directly promotes the proliferation of some kinds of tumor cells. Also activating immunosuppressive cells, it supports immune escape and tumor development.
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.
Both CD4+ and CD8+ human Treg cells were most efficiently expanded in the presence of TNFRII activation.
this paper shows association of TNFRSF1B promoter polymorphisms with autoimmune diseasse
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.
Data suggest that an autocrine tumor necrosis factor-alpha (TNFalpha)-tumor necrosis factor receptor 2 (TNFR2) loop plays an important role in endorsing Treg cell stability.
It can be concluded that the mRNA levels of TNFR1 and TNFR2 were not associated with coronary artery disease risk
In rotenone-mediated dopaminergic cell models, the enhancement of p75 contributed to alpha-syn expression. The elevation of p75 also boosts the expression of ubiquitin ligase absentia homolog (siAH) and nuclear p65. Thus, p75 may enhance alpha-syn expression by promoting the activation of siAH, which is associated with ubiquitination.
The soluble TNF-RII/I ratio increased profoundly as macrophage activation syndrome developed and correlated positively with disease activity
The aim of current study was to explore longitudinally the prevalence, severity, potential factors, and predictors of depression among Chinese Han adolescent survivors with different genotypes of tumor necrosis factor receptor-II (TNF-RII) rs1061622 after the 2008 Wenchuan earthquake
The case-control study (401 patients and 657 controls) revealed that the genetic variants of rs3397, rs1061622, and rs1061624 in the TNFR2 gene are associated with a higher risk of developing schizophrenia and more severe course in men.
Elevated TNFRs levels were associated with the risk of cardiovascular and/or all-cause mortality independent of all relevant covariates in patients undergoing haemodialysis
TL1A modulated Rheumatoid arthritis-fibroblast-like synoviocytes migration and Indian hedgehog signaling pathway using TNFR2.
These results show an unclear effect of considered T>C polymorphism on TNF-RII gene expression in bovine leukocytes and they suggest the involvement of BLV in modifying the TNF-RII expression in BLV-infected cows.
These results suggest that the endometrium might lower the TNF concentration in the blastocyst by (1) regulating TNF secretion into the uterine fluid and (2) inducing decreased TNF and TNFR2 mRNA transcription in the embryo.
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.[TNFRII]
Retinal ischemia results in increased expression of TNF-alpha and its receptors (TNF-R1 and TNF-R2).
Porcine TNFR2 (1,125 bp, 375 amino acid residues), which contains specific amino acid region of transmembrane, indicated high identities with human and murine TNFR2
pTNFR2 isoforms may play differential roles in the process of xenograft rejection.
Study data indicate a pleiotropy of Tnfr2 functions, with mesenchymal Tnfr2 driving cell activation and arthritis/valve stenosis pathogenesis only in the presence of systemic Tnfr2, whereas nonmesenchymal Tnfr2 overcomes this function, providing protective signals and, thus, containing both pathologies.
TNF-induced pathology was induced specifically through the TNFR1 receptor, while TNFR2-mediated signaling was distinctly protective in colitis and ankle joint inflammation. Overall, our data show that TNF is a critical modulator of pyrin expression, inflammasome activation, and pyrin-inflammasomopathy.
Selective activation of TNFRII was found to expand both CD4+ and CD8+ Treg cells. TNFRII activation elevated the number of CD4+CD25+ and CD8+CD25+ Treg cells and increased the number of FoxP3-expressing cells in CD8+, but not CD4+, Treg cells. In the experimental arthritis model, TNFRII activation led to the expansion of both CD4+ and CD8+ Treg cells in vivo and induced antiinflammatory responses that alleviated arthritis
Toll like receptor-4 (TLR4) and tumor necrosis factor receptor type II (TNFR2)-dependent mechanisms, but not IL-10-dependent pathways, modulate the anti-inflammatory response of CD4+ Tregs following trauma.
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.
MPTP induced TNF-alpha signaling through TNFR2 mediated pathway and recruited p65-p52 dimer in hippocampal nucleus which is reported to have protective effect on hippocampal neurons indicated by unchanged neuronal count in hippocampus in treated groups with respect to control.
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.
TNFR2 sensitizes macrophages for endogenous TNF-induced TNFR1-mediated necroptosis
study reports an important role for TNFR2 on low-affinity-primed secondary effector CD8+ T cells; results demonstrate the importance of TNF signaling in low-affinity, cross-reactive CD8+ T cell responses during heterologous immunity
TNF plays an inhibitory role in modulating myocardial SDF-1 production and blockade of TNF signaling by ablation of TNFR1 and TNFR2 genes increased SDF-1 expression in the heart. These data expand on TNF signaling-initiated mechanisms in myocardium, which may lend a more complete understanding of SDF-1 and TNFR-derived actions in hopes of advancing ischemic heart injury treatments.
Results suggest that elevated TNF in the heart, via TNFR1 and TNFR2, restrains cardiomyocyte differentiation of resident cardiac stem cells and may enhance adrenergic activation, both effects that would reduce the effectiveness of endogenous cardiac repair and the response to exogenous stem cell therapy, while promoting adverse cardiac remodeling.
Report chronic inflammatory multiorgan hepatobiliary pancreatitis, along with fibrosis and calculi formation induced by oral dibutyltin administration in TNFR1/R2 deficient mice.
These findings implicate TNF-receptor signaling cascades in the regulation of homeostatic plasticity of denervated networks and suggest an important role for TNFalpha-signaling in the course of neurological diseases accompanied by deafferentation.
TNF receptor 1 (TnfR1) signaling is believed to be a major mediator of the cytotoxicity of Tnf-a through activation of caspases.
our findings implicate TNFR2 in supporting myeloid-derived suppressor cells -mediated immune suppression and metastasis in the liver
TNFR2 blockade appears to disrupt commensal bacteria-host immune symbiosis to reveal autoimmune demyelination in genetically susceptible mice.
TNFR2 protects mice from colitis by inhibiting the expansion of colonic CD8(+) T cells.
Collectively, these results demonstrate that TNFR2-bearing CD8(+) T cells and TNFR1-bearing non-CD8(+) T cells contribute significantly to oviduct pathology following genital chlamydial infection.
To determine the role of TNF-TNFR2/p75 signaling in ischemia-induced inflammation and muscle regeneration, we subjected wild-type and TNFR2/p75 knockouts to hind limb ischemia.
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.
The protein encoded by this gene is a member of the TNF-receptor superfamily. This protein and TNF-receptor 1 form a heterocomplex that mediates the recruitment of two anti-apoptotic proteins, c-IAP1 and c-IAP2, which possess E3 ubiquitin ligase activity. The function of IAPs in TNF-receptor signalling is unknown, however, c-IAP1 is thought to potentiate TNF-induced apoptosis by the ubiquitination and degradation of TNF-receptor-associated factor 2, which mediates anti-apoptotic signals. Knockout studies in mice also suggest a role of this protein in protecting neurons from apoptosis by stimulating antioxidative pathways.
, p75 TNF receptor
, p80 TNF-alpha receptor
, soluble TNFR1B variant 1
, tumor necrosis factor beta receptor
, tumor necrosis factor binding protein 2
, tumor necrosis factor receptor 2
, tumor necrosis factor receptor superfamily member 1B
, tumor necrosis factor receptor type II
, tumor necrosis factor receptor-II
, tumor necrosis factor receptor superfamily, member 1B
, TNF receptor beta chain
, p75 TNFR