OBJECTIVE: To determine whether selective blockade of tumor necrosis factor receptor I (TNFRI) affects spontaneous proinflammatory cytokine and chemokine production in ex vivo-cultured human rheumatoid arthritis synovial membrane mononuclear cells (MNCs) and to compare this response to that of TNF

Tumor Necrosis Factor Receptor I (TNFRI) is a 55 kDa pleiotropic cytokine that is considered a primary modifier of the inflammatory and immune reactions of

We have shown that high plasma levels of sTNFR1 during the acute phase are associated with long-term all-cause mortality and cardiovascular death in HF following AMI. Previously, Rauchhaus et al. (7) reported that sTNF-R1 emerged among all cytokine parameters as the strongest and most accurate prognostic marker in chronic HF. Recently, Valgimigli et al. (8) reported that among several inflammatory markers, sTNF-R1 remained the only independent predictor of death and HF after MI. The present study confirms and extends these findings, evaluating the prognostic significance of raised plasma sTNF-R1 in HF both in the acute phase and during follow-up. In fact, we show that non-survivors have raised plasma levels of sTNFR1 compared with survivors not only at baseline but at all time points during the observation period. Importantly, we show that sTNF-R1 has predictive power independent of other well-established risk markers such as N-BNP and hsCRP (9), possibly reflecting that we are focusing on a ...

Studies of tumour necrosis factor receptor-1 in tumour necrosis factor receptor associated periodic sysndrome (TRAPS): United Kingdom

article{44794e1d-6590-4011-af20-61016be2fcd3, abstract = {Inflammation and ischemia have a synergistic damaging effect in the immature brain. The role of tumor necrosis factor (TNF) receptors 1 and 2 in lipopolysaccharide (LPS)-induced sensitization and tolerance to oxygen-glucose deprivation (OGD) was evaluated in neonatal murine hippocampal organotypic slices. Hippocampal slices from balb/c, C57BL/6 TNFR1(-/-), TNFR2(-/-), and wild-type (WT) mice obtained at P6 were grown in vitro for 9 days. Preexposure to LPS immediately before OGD increased propidium iodide-determined cell death in regions CA1, CA3, and dentate gyrus from 4 up to 48 h after OGD (P<0.001). Extending the time interval between LPS exposure and OGD to 72 h resulted in tolerance, that is reduced neuronal cell death after OGD (P<0.05). Slices from TNFR1(-/-) mice showed neither LPS-induced sensitization nor LPS-induced tolerance to OGD, whereas both effects were present in slices from TNFR2(-/-) and WT mice. Cytokine ...

PE anti-mouse CD120a (TNF R Type I/p55) Antibody - CD120a is a 55 kD Type I transmembrane protein, also known as Tumor Necrosis Factor Receptor Type I (TNFRI) or p55.

The CD27 antigen is a transmembrane glycoprotein disulfide-linked homodimer composed of 55 kDa monomers. CD27 belongs to the Tumor Necrosis Factor Receptor (TNFR) gene family. CD27 antigen is found on medullary thymocytes, peripheral T lymphocytes, activated B lymphocytes and NK cells. It is preferentially expressed on the CD45RA+ CD45R0 -, naïve subset of CD4+ T lymphocytes. Its ligand is CD70 ...

TY - JOUR. T1 - Efficacy of etanercept in the tumor necrosis factor receptor-associated periodic syndrome. T2 - A prospective, open-label, dose-escalation study. AU - Bulua, Ariel C.. AU - Mogul, Douglas B.. AU - Aksentijevich, Ivona. AU - Singh, Harjot. AU - He, David Y.. AU - Muenz, Larry R.. AU - Ward, Michael M.. AU - Yarboro, Cheryl H.. AU - Kastner, Daniel L.. AU - Siegel, Richard M.. AU - Hull, Keith M.. PY - 2012/3. Y1 - 2012/3. N2 - Objective To investigate the efficacy of etanercept in improving the symptoms and underlying inflammation in patients with tumor necrosis factor receptor-associated periodic syndrome (TRAPS). Methods Fifteen patients with TRAPS were enrolled in a prospective, open-label, dose-escalation study. Patients recorded attacks, symptom severity, and use of ancillary medications in a daily diary. Blood samples were collected during each period and measured for levels of acute-phase reactants. Between 7 years and 9 years after the conclusion of the initial study, ...

Tumor Necrosis Factor Receptor Superfamily Member 1A (Tumor Necrosis Factor Receptor 1 or Tumor Necrosis Factor Receptor Type I or p55 or p60 or CD120a - Market research report and industry analysis - 12355963

Tumour necrosis factor-alpha receptor 1 and 2 polymorphisms in inflammatory bowel disease and their association with response to infliximab ...

|p|Tumor necrosis factor receptor superfamily, member 1A is a member of the Tumor necrosis factor receptor superfamily, which also contains TNFRSF1B. This protein is one of the major receptors for the tumor necrosis factor-alpha. This receptor can activate the transcription factor NF-kB, 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 human genetic disorder called periodic fever syndrome. Impaired receptor clearance is thought to be a mechanism of the disease.|/p|

TY - JOUR. T1 - Wengen, a member of the Drosophila tumor necrosis factor receptor superfamily, is required for eiger signaling. AU - Kanda, Hiroshi. AU - Igaki, Tatsushi. AU - Kanuka, Hirotaka. AU - Yagi, Takeshi. AU - Miura, Masayuki. PY - 2002/8/9. Y1 - 2002/8/9. N2 - We identified Wengen, the first member of the Drosophila tumor necrosis factor receptor (TNFR) superfamily. Wengen is a type III membrane protein with conserved cysteine-rich residues (TNFR homology domain) in the extracellular domain, a hallmark of the TNFR superfamily. wengen mRNA is expressed at all stages of Drosophila development. The small-eye phenotype caused by an eye-specific overexpression of a Drosophila TNF superfamily ligand, Eiger, was dramatically suppressed by down-regulation of Wengen using RNA interference. In addition, Wengen and Eiger physically interacted with each other through their TNFR homology domain and TNF homology domain, respectively. These results suggest that Wengen can act as a component of a ...

Short gene description: Tumor necrosis factor receptor superfamily member 1B Precursor (Tumor necrosis factor receptor 2)(TNF-R2)(Tumor necrosis factor receptor type II)(p75)(p80 TNF-alpha receptor)(CD120b antigen)(Etanercept) [Contains Tumor necrosis factor receptor superfamily member 1b, membrane form;Tumor necrosis factor-binding protein 2(TBPII)(TBP-2)] [Source:UniProtKB/Swiss-Prot;Acc:P20333 ...

TNF-alpha and lymphotoxin alpha (TNF-beta) are pleiotropic cytokines with regulatory functions in inflammatory reactions and T cell activation. Natural TNF inhibitors such as soluble TNF-binding proteins, i.e. TNFsR55 and TNFsR75, are shed from white blood cells and probably other cells. These naturally occurring inhibitors of TNF are shown to be 10 times less effective than the bivalent antagonist of TNF, recombinant soluble TNF receptor p55-human gamma 3 fusion protein (rsTNFR-p55h gamma 3), in controlling the release of prostaglandin E2 (PGE2) and collagenase by fibroblasts, as well as in controlling T cell proliferation. In order to block the action of rhTNF-alpha added to fibroblasts, a fivefold excess of rsTNFR-p55h gamma 3 was sufficient, but concentrations of a hundred to a thousand times higher were required to obtain a significant inhibition of T cell activation. This concentration appears to be required to block membrane-bound TNF-alpha on peripheral blood mononuclear cells

Vaccinia virus (VACV), the smallpox vaccine, encodes many proteins that subvert the host immune response. One of these, cytokine response modifier E (CrmE), is secreted by infected cells and protects these cells from apoptotic challenge by tumour necrosis factor alpha (TNFalpha). We have expressed recombinant CrmE from VACV strain Lister in Escherichia coli, shown that the purified protein is monomeric in solution and competent to bind TNFalpha, and solved the structure to 2.0 A resolution. This is the first structure of a virus-encoded tumour necrosis factor receptor (TNFR). CrmE shares significant sequence similarity with mammalian type 2 TNF receptors (TNFSFR1B, p75; TNFR type 2). The structure confirms that CrmE adopts the canonical TNFR fold but only one of the two ligand-binding loops of TNFRSF1A is conserved in CrmE, suggesting a mechanism for the higher affinity of poxvirus TNFRs for TNFalpha over lymphotoxin-alpha. The roles of dimerisation and pre-ligand-assembly domains (PLADs) in poxvirus

Intracellular pathogens, such as M. tuberculosis , have developed strategies for subverting microbicidal mechanisms and living within the host macrophage. However, a variety of signals, such as those mediated by the cytokines IFN-g and TNF-a, or by components of the mycobacterial cell wall, can activate macrophages to produce antimicrobial mediators, such as nitric oxide (NO). Conversely, as M. tuberculosis replicates within the macrophage, it can itself become toxic to the macrophage. The ultimate outcome of this relationship---destruction of bacilli by the macrophage, or successful parasitism of the macrophage by the bacillus---depends, in part, on the ability of the macrophage to become activated before lysis occurs. Thus, a better understanding of the signals and signal transduction pathways which control macrophage activation in response to infection will yield insights into the relationship between M. tuberculosis and its host.;One mechanism which may regulate macrophage activation and ...

TY - JOUR. T1 - Ligand-induced formation of p55 and p75 tumor necrosis factor receptor heterocomplexes on intact cells. AU - Pinckard, J. Keith. AU - Sheehan, Kathleen C F. AU - Schreiber, Robert D.. N1 - Copyright: Copyright 2007 Elsevier B.V., All rights reserved.. PY - 1997/4/18. Y1 - 1997/4/18. N2 - The p55 and p75 tumor necrosis factor receptors are known to mediate their effects on cells through distinct signaling pathways. Under certain circumstances, the two classes of TNF receptors cooperate with each another to produce enhanced cellular responses. The only molecular mechanism proposed thus far to explain this effect is the process of ligand passing, whereby TNF is concentrated at cell surfaces by binding to p75 and then following dissociation from this receptor class binds with high efficiency to p55. Using the in vivo model of TNF-induced TNF receptor shedding we have uncovered a novel ligand-dependent interaction of the two TNF receptors that occurs upon exposure of cells to TNF. ...

TY - JOUR. T1 - TNF receptor I is required for induction of macrophage heat shock protein 70. AU - Heimbach, Julie K.. AU - Reznikov, Leonid L.. AU - Calkins, Casey M.. AU - Robinson, Thomas N.. AU - Dinarello, Charles A.. AU - Harken, Alden H.. AU - Meng, Xianzhong. PY - 2001. Y1 - 2001. N2 - Expression of heat shock proteins (HSP) is an adaptive response to cellular stress. Stress induces tumor necrosis factor (TNF)-α production. In turn, TNF-α induces HSP70 expression. However, osmotic stress or ultraviolet radiation activates TNF-α receptor I (TNFR-I) in the absence of TNF-α. We postulated that TNF-α receptors are involved in the induction of HSP70 by cellular stress. Peritoneal Mφ were isolated from wild-type (WT), TNF-α knockout (KO), and TNFR (I or II) KO mice. Cells were cultured overnight and then heat stressed at 43 ± 0.5°C for 30 min followed by a 4-h recovery at 37°C. Cellular HSP70 expression was induced by heat stress or exposure to endotoxin [lipopolysaccharide (LPS)] as ...

Execution of apoptosis is a regulated mechanism involving several components. The extrinsic and intrinsic pathways are the two most extensively studied apoptotic pathways. In the extrinsic pathway, caspase activation is initiated at membrane bound death receptor (DR) molecules that belong to the tumor necrosis factor (TNF) receptor superfamily [161718]. To date, eight death receptors have been characterized: tumor necrosis factor receptor-1 (TNFR1, also known as DR1), Fas (CD95/APO-1), TNF related apoptosis inducing ligand receptor-1 (TRAIL R1/DR4), TRAIL R2/DR5, DR3 (APO-3/TRAMP), DR6, nerve growth factor receptor (NGFR), and ectodysplasin A receptor (EDAR) [19]. Each of these have corresponding ligand molecules that belong to the TNF family of proteins, including TNF-α [20], Fas ligand (FasL/CD95L) [21], TNF related apoptosis inducing ligand (TRAIL) [22], and APO-3 ligand (APO-3L) [23]. The extrinsic pathway is invoked when death associated ligands bind to their respective death receptors. ...

One of the earliest TNF-dependent events to occur during liver regeneration is the activation of the transcription factor NF-κB through TNF receptor type 1. NF-κB activation in the liver can have both antiapoptotic and ...

View mouse Tnfrsf18 Chr4:156026164-156028895 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression

View mouse Tnfrsf13b Chr11:61126755-61149372 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression

The KOMP Repository is located at the University of California Davis and Childrens Hospital Oakland Research Institute. Question? Comments? For Mice, Cells, and germplasm please contact us at [email protected], US 1-888-KOMP-MICE or International +1-530-752-KOMP, or for vectors [email protected] or +1-510-450-7917 ...

The KOMP Repository Collection is located at the MMRRC at the University of California, Davis and Childrens Hospital Oakland Research Institute. Question? Comments? For Mice, Cells, and germplasm please contact us at [email protected], US 1-888-KOMP-MICE or International +1-530-752-KOMP, or for vectors [email protected] or +1-510-450-7917 ...

These reference sequences exist independently of genome builds. Explain. These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above. ...

The HB14 monoclonal antibody reacts with human CD40, a 45-50 kDa type I transmembrane glycoprotein and member of the tumor necrosis factor receptor (TNFR) superfamily. It is expressed primarily on B cells, macrophages, follicular dendritic cells, endothelial cells, and fibroblasts and at lower levels on plasma cells and a subset of peripheral T cells. CD40 is involved in B cell differentiation and proliferation, isotype class-switching, and protection of B cells from apoptosis. Interaction of CD40 with its ligand CD154 is important in T cell-B cell interaction and plays a role in costimulation and immune regulation. Clone HB14 blocks the binding of CD40 to CD154. This prevents down-regulation of CD154 expression induced by interaction with CD40 expressed on antigen-presenting cells. - Belgique

Clone FGK45.5 recognizes the mouse CD40 antigen, a 40-50 kDa glycoprotein and member of the tumor necrosis factor receptor (TNFR) superfamily. CD40 is expressed on B lymphocytes, macrophages, and dendritic cells and is an important costimulatory molecule for B cells as well as dendritic cells, monocytes, and other antigen-presenting cells (APCs). The interaction of CD40 on B cells with its ligand CD154 is involved in B cell activation and differentiation; engagement of CD40 on dendritic cells leads to maturation. Clone FGK45 can be used for blocking of CD40/CD154 interaction and for in vitro and in vivo activation of CD40-expressing APCs. - USA

WORKLIST ENTRIES (1): TNFACTORR14 View alignment Tumour necrosis factor receptor 14 signature Type of fingerprint: COMPOUND with 4 elements Links: PRINTS; PR01918 TNFACTORR1A; PR01919 TNFACTORR1B; PR01920 TNFACTORR3 PRINTS; PR01921 TNFACTORR4; PR01922 TNFACTORR5; PR01680 TNFACTORR6 PRINTS; PR01960 TNFACTORR7; PR01923 TNFACTORR8; PR01924 TNFACTORR9 PRINTS; PR01956 TNFACTORR10; PR01961 TNFACTORR11; PR01962 TNFACTORR12 PRINTS; PR01963 TNFACTORR13B; PR01964 TNFACTORR13C; PR01966 TNFACTORR16 PRINTS; PR01967 TNFACTORR17; PR01968 TNFACTORR18; PR01969 TNFACTORR19 PRINTS; PR01970 TNFACTORR19l; PR01971 TNFACTORR21; PR01972 TNFACTORR25 PRINTS; PR01973 TNFACTORR27 PRINTS; PR01974 TNFACTORR11A; PR01975 TNFACTORR11B MIM; 602746 Creation date 23-JUN-2009 1. ARMITAGE, R. Tumor necrosis factor receptor superfamily members and their ligands. CURR.OPIN.IMMUNOL. 6 407-413 (1994). 2. BANNER D., DARCY, A., JAMES, W., GENTZ, R., SCHOENFELD, H., BROGER, C., LOETSCHER, H. AND LESSLAUER, W. Crystal structure of the ...

specificalPrinciple of the assay: mouse TNFRSF14 ELISA Kit was based on standard sandwich enzyme-linked immune-sorbent assay technology. A monoclonal antibody from rat specific for TNFRSF14 has been precoated onto 96-well plates. Standards(CHO, Q29-V207) and test samples are added to the wells, a biotinylated detection polyclonal antibody from goat specific for TNFRSF14 is added subsequently and then followed by washing with PBS or TBS buffer. Avidin-Biotin-Peroxidase Complex was added and unbound conjugates were washed away with PBS or TBS buffer. HRP substrate TMB was used to visualize HRP enzymatic reaction. TMB was catalyzed by HRP to produce a blue color product that changed into yellow after adding acidic stop solution. The density of yellow is proportional to the mouse TNFRSF14 amount of sample captured in plate. Background: Tumor necrosis factor receptor superfamily member 14 (TNFRSF14), also known as HVEM, is a protein that in humans is encoded by the TNFRSF14 gene. The protein encoded ...

TNFRSF9 - TNFRSF9 (untagged)-Human tumor necrosis factor receptor superfamily, member 9 (TNFRSF9) available for purchase from OriGene - Your Gene Company.

Full text for this publication is not currently held within this repository. Alternative links are provided below where available. ...

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https://doi.org/10.18632/oncotarget.15461 Linlin Wang, Dong Yang, Jing Tian, Aiqin Gao, Yihang Shen, Xia Ren, Xia Li, Guosheng Jiang, Taotao Dong

BAFF/BLyS, a member of the tumor necrosis family (TNF) superfamily of ligands, is a crucial survival factor for B cells. BAFF binds three receptors, TACI, BCMA, and BR3, with signaling through BR3 being essential for promoting B cell function. Typical TNF receptor (TNFR) family members bind their cognate ligands through interactions with two cysteine-rich domains (CRDs). However, the extracellular domain (ECD) of BR3 consists of only a partial CRD, with cysteine spacing distinct from other modules described previously. Herein, we report the solution structure of the BR3 ECD. A core region of only 19 residues adopts a stable structure in solution. The BR3 fold is analogous to the first half of a canonical TNFR CRD but is stabilized by an additional noncanonical disulfide bond. BAFF-binding determinants were identified by shotgun alanine-scanning mutagenesis of the BR3 ECD expressed on phage. Several of the key BAFF-binding residues are presented from a beta-turn that we have shown previously to ...

Recent studies have shown that the tumor necrosis factor (TNF) system is implicated in the insulin resistance of human obesity. Plasma concentrations of the soluble fraction of the TNF receptors 1 and 2 (sTNFR1 and sTNFR2) are thought to reflect the degree of activation of the TNF system. The purpose of this study was to explore whether this activation, as measured by the levels of circulating sTNFR1 and sTNFR2, is associated with insulin resistance. A total of 19 men (mean age 36.2 +/- 1.9; BMI 28.8 +/- 1.2, range 22.2-35.7) and 17 premenopausal women (age 34.9 +/- 1.4; BMI 28.1 +/- 0.8, range 19-37.9) were studied. Men showed higher levels of plasma sTNFR1 and sTNFR2 than women. However, obese men showed increased levels of sTNFR2 but similar levels of sTNFR1 in comparison with obese women. In fact, sTNFR2 levels correlated with BMI (r = 0.50, P = 0.002), fat-free mass (FFM) (r = 0.61, P , 0.0001), and waist-to-hip ratio (WHR) (r = 0.39, P = 0.02), but not with fat mass or percent fat mass. ...

A method, and system, to induce remission in diseases characterized by excess production of sTNR and interleukin 2 has been developed. In the most preferred embodiment, the system consists of antibodies to sTNFR1, sTNFR2 and sIL2R immobilized in a column containing a material such as SEPHAROSE™. The patient is connected to a pheresis machine which separates the blood into the plasma and red cells, and the plasma is circulated through the column until the desired reduction in levels of sTNFR1, sTNFR2, and IL2 is achieved, preferably to less than normal levels. In the preferred method, patients are treated three times a week for four weeks. This process can be repeated after a period of time. Clinical studies showed reduction in tumor burden in patients having failed conventional chemotherapy and radiation treatments.

Acts as a lipid transfer protein. Preferentially captures and shuttles two lipid second messengers, i.e., phosphatidylinositol 4,5- bisphosphate and phosphatidylinositol 3,4,5-trisphosphate and increases their levels in the plasma membrane. Additionally, may also function as a lipid-presenting protein to enhance the activity of the PI3K-AKT and MEK-ERK pathways. May act as a regulator of tumorigenesis through its activation of phospholipid signaling ...

TRAF-STOP inhibitor 6877002，一种抑制 CD40-TRAF6 相互作用的选择性抑制剂，从专利 WO2014033122A1 中获得，抑制 RAW 细胞中 NF-κB 活化，化合物VII。TRAF-STOP 6877002 可阻止小鼠中已发生的动脉粥样硬化恶化，减少白细胞募集并减少巨噬细胞活化；减少动脉粥样硬化斑块中的巨噬细胞增殖。- 高纯度，全球文献引用。

TNFRSF18 входит в многочисленное надсемейство рецепторов факторов некроза опухоли (TNFR). Экспрессия этого рецептора повышается при активации T-лимфоцитов. Играет ключевую роль в доминантной иммунологической аутотолерантности, обеспечиваемой регуляторными CD25+/CD4+ T-лимфоцитами. Исследования с нокаутными мышами показали роль этого рецептора в регуляции CD3-опосредуемых активации T-лимфоцитов и апоптозе.[1] Участвует в связывании лейкоцитов с эндотелиальными клетками. Активирует фактор транскрипции NF-κB через сигнальный путь TRAF2/NIK.[2] Участвует в ...

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Levels of soluble tumour necrosis factor receptors (sTNFRs) are elevated in the circulation of patients with rheumatoid arthritis (RA). Although these receptors can act as natural inhibitors of tumour necrosis factor-α, levels of sTNFRs in RA appear to be insufficient to prevent tumour necrosis factor-α induced inflammation. The factors that regulate circulating levels of sTNFRs are unclear, but polymorphisms in the tumour necrosis factor receptor genes may play a role. We investigated the relationship between polymorphisms in the tumour necrosis factor receptor I (TNF-RI) and II (TNF-RII) genes and levels of sTNFRs in two groups of Caucasian RA patients: one with early (disease duration ≤2 years; n = 103) and one with established disease (disease duration ≥5 years; n = 151). PCR restriction fragment length polymorphism analysis was used to genotype patients for the A36G polymorphism in the TNF-RI gene and the T676G polymorphism in TNF-RII. Levels of sTNFRs were measured using ELISA. We also

A Tumor Necrosis Factor Family member that is released by activated Lymphocytes. Soluble lymphotoxin is specific for Tumor Necrosis Factor Receptor Type I; Tumor Necrosis Factor Receptor Type II; and Tumor Necrosis Factor Receptor Superfamily, Member 14. Lymphotoxin-alpha can form a Membrane-bound heterodimer with Lymphotoxin-beta that has specificity for the Lymphotoxin beta Receptor ...

Background: The tumor necrosis factor alpha (TNFα) is a cytokine that produced principally by monocyte/macrophages and T lymphocytes, respectively. TNFα is recognized as the primary mediator of immunity in inflammation reaction. One important application of Tumor Necrosis Factor Receptor 2 (TNFR2) is for the treatment of autoimmune diseases like rheumatoid arthritis (RA). Objectives: The aim of this study is to examine the therapeutic trace of the recombinant humanTNFR2 on collagen-induced arthritis (CIA) in mice. Materials and Methods: CIA was created in 20 mice by immunization with bovine type II collagen (CII). After the mice were boosted on day 21, they were injected with the recombinant protein in test group (1 mg.kg-1) and assessed edema in paws and knee joints after two weeks. The quantities of inflammatory cytokines such as TNF-α, interleukin-1 beta (IL-β1), interleukin-6 (IL-6), and interleukin-10(IL-10) in serum were evaluated through enzyme-linked immunosorbent assay (ELISA) kit. In

Vaitla, P. M., Radford, P. M., Tighe, P. J., Powell, R. J., McDermott, E. M., Todd, I. and Drewe, E., Role of interleukin-6 in a patient with tumor necrosis factor receptor-associated periodic syndrome: assessment of outcomes following treatment with the anti-interleukin-6 receptor monoclonal antibody tocilizumab. Arthritis Rheum. 2011. 63: 1151-1155 ...

The flavonoids comprise a large class of low-molecular-weight plant metabolites ubiquitously distributed in food plants. These dietary antioxidants exert significant antitumor, antiallergic, and anti-inflammatory effects. The molecular mechanisms of their biological effects remain to be clearly understood. We investigated the anti-inflammatory potentials of a safe, common dietary flavonoid component, quercetin, for its ability to modulate the production and gene expression of the proinflammatory cytokine tumor necrosis factor alpha (TNF-α) by human peripheral blood mononuclear cells (PBMC). Our results showed that quercetin significantly inhibited TNF-α production and gene expression in a dose-dependent manner. Our results provide direct evidence of the anti-inflammatory effects of quercetin by PBMC, which are mediated by the inhibition of the proinflammatory cytokine TNF-α via modulation of NF-κβ1 and Iκβ. ...

Utilizado en el tratamiento de la artritis reumatoide y la reducción de los efectos adversos del factor de necrosis tumoral (TNF). TNF es una citoquina natural que interviene en inflamatoria normal y la respuesta inmune. Los niveles elevados de TNF se encuentran en los tejidos y fluidos de los pacientes con artritis reumatoide, artritis psoriásica, la espondilitis anquilosante (AS), y psoriasis en placa. Etanercept se une específicamente al factor de necrosis tumoral (TNF) y bloquea su interacción con los receptores de la superficie celular TNF ...

[65 Pages Report] Check for Discount on Tumor Necrosis Factor Receptor Superfamily Member 4 (ACT35 Antigen or TAX Transcriptionally Activated Glycoprotein 1 Receptor or OX40L Receptor or CD134 or TNFRSF4) - Pipeline Review, H1 2018 report by Global Markets Direct. Tumor Necrosis Factor Receptor Superfamily Member 4 (ACT35 Antigen or...

TY - JOUR. T1 - Role of tumor necrosis factor in preovulatory follicles of swine. AU - Prange-Kiel, J.. AU - Kreutzkamm, C.. AU - Wehrenberg, U.. AU - Rune, G. M.. PY - 2001. Y1 - 2001. N2 - The effects of tumor necrosis factor (TNF) on cultured porcine granulosa cells that were obtained from preovulatory follicles were studied with regard to following parameters: 1) TNF receptor type I expression, 2) progesterone receptor and transforming growth factor β receptor type II (TβR II) as markers of luteinization, 3) proliferation, and 4) apoptosis. For comparative purposes the effects of TNF were also studied on insulin/forskolin-treated cells, as this treatment is well established to induce luteinization. Cytochemical methods followed by semiquantitative analysis were used. Our data show that TNF treatment upregulates TNF receptor type I expression in granulosa cells. TNF downregulates the expression of TβR II of insulin/forskolin-stimulated and of unstimulated cells. The progesterone receptor ...

RA is a multigene disorder with genetic polymorphisms influencing a wide spectrum of its clinical presentations. Disease progression, pattern of joint disease, and extra-articular manifestations are highly variable.6 Several data suggested also that RA is histopathologically heterogeneous.2,3 Histological analyses in this and in previous studies showed that most rheumatoid synovia are characterised by differences in the density of the diffuse infiltrate of mononuclear cells, and lack any further specific microanatomical organisation. Such synovia may be classified as diffuse synovitis.3 In about one third of RA synovia, categorised as follicular synovitis, the formation of lymphoid conglomerates was demonstrated.2,3 The presence of lymphoid follicles was associated with a greater degree of immunological activation, and greater potential for joint tissue destruction.2-5 All these findings support the concept of the clinical and histological heterogeneity of RA.. Mononuclear cells infiltrating the ...

Tumor necrosis factor alpha (TNF-α) is important in resistance to various microorganisms and provides signals to the target cells through two different receptors, TNF-α receptor I (TNFRI) (p55 receptor) and TNFRII (p75 receptor). To delineate the significance of the two different signaling pathways in resisting infections with extracellular bacteria, we examined the resistance of mice to Streptococcus pneumoniae (serotype 6B). TNF-α needs to be present early in infections, since one injection of wild-type mice with anti-TNF-α leads to an increased susceptibility of these mice to S. pneumoniae. TNF-α signaling through the p55 receptor (but not the p75 receptor) is crucial in resisting S. pneumoniae infections, because intraperitoneal injection of 100 CFU/mouse killed p55-deficient mice by day 2 of infection, whereas 1,000,000 CFU/mouse was needed to kill half of the control mice. p55-deficient mice do not show evidence of a deficient acute- phase response. All three types of mice (p55 ...

Supported by the National Center for Advancing Translational Sciences of the National Institutes of Health under Award number UL1TR002378. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. KL2 Scholars should also list KL2TR002381 and TL1 Trainees should also list TL1TR002382 ...

Tnfrsf1a (untagged) - Mouse tumor necrosis factor receptor superfamily, member 1a (cDNA clone MGC:6117 IMAGE:3585060), (10ug), 10 µg.

Increased soluble Tumour Necrosis Factor-alpha receptors (sTNF-aR) 1 and 2 have been associated with Diabetic Kidney Disease (DKD) in type 1 and type 2 diabetes1 2 . Whether this applies to prgnancy is not known. We measured serial levels of sTNF-aR1 and 2 (R1+R2) pre, during 2nd trimester (T2) and post pregnancy in healthy women and women with pre-existing diabetes using the Multiplex immunoassay.. At baseline, estimated glomerular filtration rate was , 90ml/min/1.72m2 in all but one case. The baseline 24 hour albumin excretion rate for diabetics and controls at baseline was [17.08±8.31] and [5.31 ±1.91] µg/min (p=0.25).. Data for the study group as a whole are shown in the figure. There was 73% of type 1 compared to 27% of type 2 diabetes participants. Using serial comparison within subjects, in the diabetes group (N=8) there was a significant increase in both R1+R2 from baseline to T2 (p =0.01). This did not return to pre-pregnancy values post partum (p, 0.05) (Figure), in contrast to ...

RPB499Hu01, CD120A; P55; TBP1; FPF; TNF-R; TNF-R-I; TNF-R55; TNFAR; TNFR1; TNFR55; TNFR60; P55-R; P60; Tumor necrosis factor receptor 1; Tumor necrosis factor-binding protein 1 | Products for research use only!

TY - JOUR. T1 - FADD/MORT1 is a common mediator of CD95 (Fas/APO-1) and tumor necrosis factor receptor-induced apoptosis. AU - Chinnaiyan, Arul M.. AU - Tepper, Clifford G. AU - Seldin, Michael F. AU - ORourke, Karen. AU - Kischkel, Frank C.. AU - Hellbardt, Stefan. AU - Krammer, Peter H.. AU - Peter, Marcus E.. AU - Dixit, Vishva M.. PY - 1996/3/1. Y1 - 1996/3/1. N2 - CD95 (Fas/APO-1) and tumor necrosis factor receptor-1 (TNFR-1) are related molecules that signal apoptosis. Recently, a number of novel binding proteins have been proposed to mediate the signaling of these death receptors. Here we report that an N-terminal truncation of one of these candidate signal transducers, FADD/MORT1, abrogates CD95-induced apoptosis, ceramide generation, and activation of the cell death protease Yama/CPP32. In addition, this dominant-negative derivative of FADD (FADD-DN) blocked TNF- induced apoptosis while not affecting NF-κB activation. FADD-DN bound both receptors, and in the case of CD95, it disrupted ...

Tumor necrosis factors (TNF) alpha and beta are structurally related cytokines that mediate a wide range of immunological, inflammatory, and cytotoxic effects. During bacterial infection of the bloodstream (sepsis), TNF-alpha induction by bacterial endotoxin is thought to be a major factor contributing to the cardiovascular collapse and critical organ failure that can develop. Despite antibiotic therapy, these consequences of sepsis continue to have a high mortality rate in humans. Here we describe a potent TNF antagonist, a TNF receptor (TNFR) immunoadhesin, constructed by gene fusion of the extracellular portion of human type 1 TNFR with the constant domains of human IgG heavy chain (TNFR-IgG). When expressed in transfected human cells, TNFR-IgG is secreted as a disulfide-bonded homodimer. Purified TNFR-IgG binds to both TNF-alpha and TNF-beta and exhibits 6- to 8-fold higher affinity for TNF-alpha than cell surface or soluble TNF receptors. In vitro, TNFR-IgG blocks completely the cytolytic ...

To evaluate the role of tumor necrosis factor (TNF alpha) in bone loss resulting from estrogen deficiency, the effects of ovariectomy were explored in six-month-old transgenic mice expressing high blood levels of a soluble TNF receptor type I (sTNFR1)-FcIgG3 fusion protein, which neutralizes TNF alpha, and in their nontransgenic littermates used as controls. These transgenic mice were identical to control mice in bone mass (evaluated by bone mineral density and content) and strength. 12 weeks after ovariectomy, the decrease in bone mass and increase in osteocalcin (marker of bone turnover) found in control mice were not observed in transgenic mice, which were not different from sham-operated mice, transgenic or not. This observation suggests a critical role for TNF alpha in the pathogenesis of bone loss induced by estrogen deficiency, a common cause of morbidity in postmenopausal women. ...

Fingerprint Dive into the research topics of The role of tumour necrosis factor-α and tumour necrosis factor receptor signalling in inflammation-associated systemic genotoxicity. Together they form a unique fingerprint. ...

Objective: To investigate the possible influence of tumour necrosis factoralpha (TNF), TNF receptor I (TNFRI) and TNF receptor II (TNFRII) gene polymorphisms on anti-TNF treatment responsiveness, stratified by autoantibody ...

Tumor necrosis factor receptor superfamily, member 19, also known as TNFRSF19 and TROY is a human gene. The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor is highly expressed during embryonic development. It has been shown to interact with TRAF family members, and to activate JNK signaling pathway when overexpressed in cells. This receptor is capable of inducing apoptosis by a caspase-independent mechanism, and it is thought to play an essential role in embryonic development. Alternatively, spliced transcript variants encoding distinct isoforms have been described. GRCh38: Ensembl release 89: ENSG00000127863 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000060548 - Ensembl, May 2017 Human PubMed Reference:. Mouse PubMed Reference:. Entrez Gene: TNFRSF19 tumor necrosis factor receptor superfamily, member 19. Robertson NG, Khetarpal U, Gutiérrez-Espeleta GA, et al. (1995). Isolation of novel and known genes from a human fetal cochlear ...

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Participants received body-weight stratified dosage of canakinumab (2 milligram/ kilogram (mg/kg) for participants equal to or less than (≤) 40 kg or 150 mg for participants more than (,) 40 kg) through subcutaneous (s.c.) route as the starting dose at baseline and monthly for 4 months. The dose was escalated at Day 8 if dose of canakinumab was not sufficient to resolve the qualifying TNF-receptor associated periodic syndrome (TRAPS) flare ...

The relevance of microenvironmental interactions that mediate pro-survival signaling in CLL is now generally accepted. This is, however, thus far mainly based on in vitro studies, and their role in vivo still remains ill-defined. Interfering with the crosstalk of CLL cells and their microenvironment and thereby depriving malignant cells from supportive factors has become an attractive novel approach for treatment.. In the study herein, we identified TNFR-1 as a pivotal player in CLL pathology. We observed significantly elevated sTNFR-1 serum levels in CLL patients, in line with results from Digel et al.16 We further showed that sTNFR-1 levels correlate with β2-microglobulin and thymidine kinase serum levels, which are indicative for tumor load as well as with OS and TAD of CLL patients. Thereby, the prognostic power of sTNFR-1 was independent of established prognostic markers. These findings are in line with observed correlations of serum sTNFR-1 and disease aggressiveness in CLL, breast, ...

Despite the critical role of TNF-α in the eradication of bacteria, excessively high levels of this cytokine may lead to tissue damage, organ failure, and death, a frequent scenario for septic patients (36). For this reason, TNF-α has been neutralized in many clinical trials in an attempt to prevent the undesirable effects of this cytokine (37). The different approaches considered have included the use of monoclonal antibodies to TNF-α (38) and the TNF receptor fused to the Fc portion of IgG (39). The outcomes of these trials, however, failed to show any significant beneficial effect on the evolution of septic patients, indicating not only that other mediators of inflammation are involved in sepsis but also that, clearly, certain levels of TNF-α are required for bacterial eradication (10, 40). TNF-α supports host antibacterial defenses through several mechanisms, including potentiation of the killing of bacteria by neutrophils and upregulation of vascular and adhesion molecules, which are ...

TNF-α is a highly pleiotrophic cytokine that plays a role in immune inflammatory response. Intracellular signaling through TNF receptors may lead to apoptosis, cell activation, and/or cell proliferation. Whereas TNFR1 signaling is clearly involved in a number of pathological states (41), the role of TNFR2 in organ pathology is not widely established. Recently, a role for TNF-α in toxic and ischemic acute renal failure has been recognized (14, 16, 26, 44, 51). The mechanisms whereby TNF-α mediates acute renal failure are not clear. We used a clinically relevant model of acute renal failure, cisplatin nephrotoxicity, to investigate the TNF-α signaling pathways during acute renal injury. Several results are noteworthy.. First, we found that the expressions of both TNFR1 and TNFR2 are upregulated after cisplatin injection. This upregulation may serve to sensitize the kidney to the effects of TNF-α. In this regard, serum levels of TNF-α in cisplatin nephrotoxicity, although increased (44), are ...

TY - JOUR. T1 - Switching leukemia cell phenotype between life and death. AU - Tucker, S.J.. AU - Rae, C.. AU - Littlejohn, A.F.. AU - Paul, A.. AU - MacEwan, D.J.. PY - 2004. Y1 - 2004. N2 - Divergent life or death responses of a cell can be controlled by a single cytokine (tumor necrosis factor α, TNF) via the signaling pathways that respond to activation of its two receptors (TNFR1 and TNFR2). Here, we show that the choice of life or death can be controlled by manipulation of TNFR signals. In human erythroleukemia patient myeloid progenitor stem cells (TF-1) as well as chronic myelogenous leukemia cells (K562), granulocyte-macrophage colony-stimulating factor primes cells for apoptosis. These death-responsive cells show prolonged TNF stimulation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase, but no NF-κB transcriptional activity as a consequence of receptor-interacting protein degradation by caspases. Conversely, cells of a proliferative phenotype display antiapoptotic ...

Alix [ALG-2 (apoptosis-linked gene 2)-interacting protein X] is a ubiquitinous adaptor protein first described for its capacity to bind to the calcium-binding protein, ALG-2. Alix regulates neuronal death in ways involving interactions with ALG-2 and with proteins of the ESCRT (endosomal sorting complex required for transport). Even though all Alix interactors characterized to date are involved in endosomal trafficking, the genuine function of the protein in this process remains unclear. We have demonstrated recently that Alix and ALG-2 form in the presence of calcium, a complex with apical caspases and with the endocytosed death receptor TNFR1 (tumour necrosis factor α receptor 1), thus suggesting a molecular coupling between endosomes and the cell death machinery.. ...

Glucocorticoid-induced TNFR family related protein (GITR, CD357 or TNFRSF18) is a member of the tumor necrosis factor receptor superfamily (TNFRSF). Like other T cell co-stimulatory TNFR family members, GITR utilizes multiple oligomerization states to regulate the initiation of downstream signaling during T cell activation by antigen presenting cells (APCs). The formation of receptor superclusters, comprised of two or more trimeric molecules, has been defined for multiple TNFRs as a means of regulating downstream signal amplification. For co-stimulatory TNFRs, like GITR, CD137 and OX40, signaling outcomes in T cells are primarily mediated via the NFκB pathway that promotes cell survival and effector cell activities in response to suboptimal T cell receptor (TCR) stimulation. It has been hypothesized that the manipulation of the oligomeric states of co-stimulatory TNFRs using antibodies may have therapeutic utility in enhancing the activity of tumor-reactive T cells, either as single agents or ...

Tumor necrosis factor receptor superfamily member 14(TNFRSF14), also known as HVEM, is a protein that in humans is encoded by the TNFRSF14 gene. The protein encoded by this gene is a member of the TNF-receptor superfamily. It is mapped to 1p36.32. HVEM plays an important role in HSV pathogenesis because it enhanced the entry of several wildtype HSV strains of both serotypes into CHO cells, and mediated HSV entry into activated human T cells. HVEM and BTLA which are form a bidirectional signaling pathway can regulate cell survival and inhibitory responses between interacting cells. HVEM as an important orchestrator of mucosal immunity integrates signals from innate lymphocytes to induce optimal epithelial Stat3 activation, which indicated that targeting HVEM with agonists could improve host defense.

Porcine tumor necrosis factor Alpha,TNFA ELISA Kit is for the quantitative detection of Porcine tumor necrosis factor Alpha,TNFA concentration in serum, plasma and other biological fluids.

RIP1/3-mediated necroptosis: tumor necrosis factor (TNF) binding to itstrimeric receptor, TNF receptor-1 (TNFR1) leads to a conformational change togenerate TNF

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Cloning of genomic DNA for tumor necrosis factor and efficient expression in CHO cells.: A genomic clone for human tumor necrosis factor (TNF-alpha) was isolate

OPG antibody (Biotin) (tumor necrosis factor receptor superfamily, member 11b) for ELISA, WB. Anti-OPG pAb (GTX18068) is tested in Human samples. 100% Ab-Assurance.

OPG antibody [13H21] (tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin)) for WB. Anti-OPG mAb (GTX53424) is tested in Mouse samples. 100% Ab-Assurance.

Tumor necrosis factor (TNF-alpha), a member of a protein family called cytokines, can be your ally or your enemy. They are manufactured by your white

Avhandlingar om TUMOR NECROSIS FACTOR A. Sök bland 89236 avhandlingar från svenska högskolor och universitet på Avhandlingar.se.

We show here that ligation of OX40 Ag, a member of the tumor necrosis factor receptor (TNF-R) family, on activated umbilical cord blood CD4(+) T cells upregulates IL-4 production at priming and thereby promotes their development into effector cells producing high levels of the type 2 cytokines IL-4, IL-5, and IL-13 ...

Bioaim Human TNF-alpha EasyTest™ ELISA Kit suitable for Plasma, Serum in human. Reliably quantify 1pg/ml of TNF-alpha. It takes 1.5 hours.

An increased level of the cytokine tumor necrosis factor alpha (TNFα) has been shown to be involved in the manifestation of both chronic pain and depression with respect to the hippocampus. Previous studies in this lab ...

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 an

Learn how this cytokine has become the target of standard therapies due to its role as one of the main pro-inflammatory agents in IBD.

Free Online Library: Killing tumors with fewer side effects. (mutant form of tumor necrosis factor) (Brief Article) by Science News; Science and technology, general Cancer Care and treatment Cancer treatment Tumor necrosis factor Research

The tumor necrosis factor (TNF) and TNF receptor (TNFR) gene superfamilies regulate numerous biological functions including cell proliferation,…

Tnf - Tnf (untagged ORF) - Rat tumor necrosis factor (TNF superfamily, member 2) (Tnf), (10 ug) available for purchase from OriGene - Your Gene Company.

TNFR2 Human produced in E.Coli is a single, non-glycosylated polypeptide chain containing 184 amino acids and having a molecular mass of 20kDa.