MarketResearchReports.biz has recently announced the addition of a market study " Tumor Necrosis Factor Receptor Superfamily Member 5 (B Cell Surface Antigen CD40 or Bp50 or CDw40 or CD40L Receptor or TNFRSF5 or CD40) - Pipeline Review, H2 2016 ", is a comparative analysis of the global market.. Tumor Necrosis Factor Receptor Superfamily Member 5 (B Cell Surface Antigen CD40 or Bp50 or CDw40 or CD40L Receptor or TNFRSF5 or CD40) - Pipeline Review, H2 2016. Summary. Global Markets Directs, Tumor Necrosis Factor Receptor Superfamily Member 5 (B Cell Surface Antigen CD40 or Bp50 or CDw40 or CD40L Receptor or TNFRSF5 or CD40) - Pipeline Review, H2 2016, provides in depth analysis on Tumor Necrosis Factor Receptor Superfamily Member 5 (B Cell Surface Antigen CD40 or Bp50 or CDw40 or CD40L Receptor or TNFRSF5 or CD40) targeted pipeline therapeutics.. The report provides comprehensive information on the Tumor Necrosis Factor Receptor Superfamily Member 5 (B Cell Surface Antigen CD40 or Bp50 or CDw40 or ...
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
[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...
|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|
HTF Market Intelligence released a new research report of 41 pages on title Tumor Necrosis Factor Receptor Superfamily Member 6 (Apo 1 Antigen or Apoptosis Mediating Surface Antigen FAS or FASLG Receptor or TNFRSF6 or CD95 or FAS) - Pipeline Review, H1 2017 with detailed analysis, forecast and strategies. The study covers key regions and important players such as KAHR medical Ltd, Silence Therapeutics Plc
Tnfrsf1a (untagged) - Mouse tumor necrosis factor receptor superfamily, member 1a (cDNA clone MGC:6117 IMAGE:3585060), (10ug), 10 µg.
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!
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 ...
This gene encodes a member of the TNF (tumor necrosis factor) receptor superfamily. The encoded protein functions in signal transduction pathways that activate inflammatory and inhibitory T-cell immune response. It binds herpes simplex virus (HSV) viral envelope glycoprotein D (gD), mediating its entry into cells. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jul 2014 ...
Research proven purified goat polyclonal TRAIL R3, DcR 1 or CD263 antibody. DcR1 is attached to the cell surface through glycophospholipid anchor. It has the extracellular TRAIL binding domain but lacks the cytoplasmic domain to induce apoptotic signal. Hence overexpression of DcR1 inhibits the TRAIL induced apoptosis. Designed for immunohistochemistry, western blotting, ELISA and related apllications. IHC image in product description.
The TNFRSF11A gene encodes a member of the TNF receptor family and is therefore involved in regulation of immunen processes. Mutations cause autosomal recessive juvenile Paget disease, osteopetrosis, and dominant familial expansile osteolysis.. ...
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Reagents, Tools and Custom Services for molecular biology, specializing in the fields of Nano-Antibody development (nAb), Cellular Reprogramming (iPSC), Genome Editing, Fluorescent Proteins, RNAi, Viral Packaging and Protein expression.
TY - JOUR. T1 - 10-Year associations between tumor necrosis factor receptors 1 and 2 and cardiovascular events in patients with stable coronary heart disease. T2 - A CLARICOR (Effect of Clarithromycin on Mortality and Morbidity in Patients with Ischemic Heart Disease) trial substudy. AU - Carlsson, Axel C.. AU - Ruge, Toralph. AU - Kjøller, Erik. AU - Hilden, Jørgen. AU - Kolmos, Hans Jørn. AU - Sajadieh, Ahmad. AU - Kastrup, Jens. AU - Jensen, Gorm Boje. AU - Larsson, Anders. AU - Nowak, Christoph. AU - Jakobsen, Janus Christian. AU - Winkel, Per. AU - Gluud, Christian. AU - Ärnlöv, Johan. N1 - © 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.. PY - 2018/4/23. Y1 - 2018/4/23. N2 - BACKGROUND: We aimed to assess the associations and predictive powers between the soluble receptors for tumor necrosis factor (TNF)-α (TNFR1 and TNFR2) and cardiovascular outcomes in patients with stable coronary heart disease.METHODS AND RESULTS: CLARICOR (Effect of ...
Nine different IgG fusion proteins and one non-fusion protein, all containing sequences from the extracellular domain of either of two human TNF receptors, were compared for their ability to bind and inhibit human TNF-alpha or TNF-beta. The fusion proteins differed with respect to TNF receptor type (p55 or p75 TNF receptor), receptor valency (one, two or four receptor domains per molecule), the presence or absence of a CH1 domain in the IgG constant region, and the proportion of the extracellular domain included in the construct. In vitro TNF binding assays and cytotoxicity assays indicated that, of the constructs that bound TNF, the greatest difference in affinity and neutralizing capability was between monovalent and bivalent receptor constructs. Differences were also noted between tetravalent and bivalent versions of p55 fusion proteins, as well as between a p75 fusion protein comprising the complete extracellular domain and one lacking the C-terminal 53 amino acids of the extracellular domain. p55
TNFRSF9 - TNFRSF9 (untagged)-Human tumor necrosis factor receptor superfamily, member 9 (TNFRSF9) available for purchase from OriGene - Your Gene Company.
TY - JOUR. T1 - Essential role of TNF receptor superfamily 25 (TNFRSF25) in the development of allergic lung inflammation. AU - Fang, Lei. AU - Adkins, Becky. AU - Deyev, Vadim. AU - Podack, Eckhard R.. PY - 2008/5/12. Y1 - 2008/5/12. N2 - We identify the tumor necrosis factor receptor superfamily 25 (TNFRSF25)/TNFSF15 pair as critical trigger for allergic lung inflammation, which is a cardinal feature of asthma. TNFRSF25 (TNFR25) signals are required to exert T helper cell 2 (Th2) effector function in Th2-polarized CD4 cells and co-stimulate interleukin (IL)-13 production by glycosphingolipid-activated NKT cells. In vivo, antibody blockade of TNFSF15 (TL1A), which is the ligand for TNFR25, inhibits lung inflammation and production of Th2 cytokines such as IL-13, even when administered days after airway antigen exposure. Similarly, blockade of TNFR25 by a dominant-negative (DN) transgene, DN TNFR25, confers resistance to lung inflammation in mice. Allergic lung inflammation - resistant, ...
A novel member of the tumor necrosis factor (TNF) cytokine family, designated TRANCE, was cloned during a search for apoptosis-regulatory genes using a somatic cell genetic approach in T cell hybridomas. The TRANCE gene encodes a type II membrane protein of 316 amino acids with a predicted molecular mass of 35 kDa. Its extracellular domain is most closely related to TRAIL, FasL, and TNF. TRANCE is an immediate early gene up-regulated by TCR stimulation and is controlled by calcineurin-regulated transcription factors. TRANCE is most highly expressed in thymus and lymph nodes but not in nonlymphoid tissues and is abundantly expressed in T cells but not in B cells. Cross-hybridization of the mouse cDNA to a human thymus library yielded the human homolog, which encodes a protein 83% identical to the mouse ectodomain. Human TRANCE was mapped to chromosome 13q14 while mouse TRANCE was located to the portion of mouse chromosome 14 syntenic with human chromosome 13q14. A recombinant soluble form of
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 ...
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
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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 worlds first wiki where authorship really matters. Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts.
The worlds first wiki where authorship really matters. Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts.
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 ...
The TNF receptor superfamily members are all type I membrane glycoproteins with typical homology in the extracellular domain of variable numbers of cysteine-rich repeats (overall homologies, 25% to 30%). In contrast, the TNF ligand superfamily members (with the exception of LT alpha) are type II membrane glycoproteins with homology to TNF in the extracellular domain (overall homologies, 20%). TNF and LT alpha are trimeric proteins and are composed of beta-strands forming a beta-jellyroll. The homology of the beta-strand regions for the TNF ligand superfamily members suggest a similar beta-sandwich structure and possible trimeric or multimeric complex formation for most or all members. A genetic linkage, as evidence for evolutionary relatedness, is found by chromosomal cluster of TNFR p80, CD30, 4-1BB, and OX40 for 1p36; TNFR p60, TNFR-RP, and CD27 for 12p13; TNF, LT alpha, and LT beta for 6 (MHC locus); CD27L and 4-1BBL for 19p13; and FASL and OX40L for 1q25. Of the TNF ligand superfamily, TNF, ...
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 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.
OBJECTIVE: Circulating soluble tumor necrosis factor receptors 1 and 2 (sTNFR1 and sTNFR2) are associated with chronic kidney disease (CKD) progression in patients with CKD or diabetes, and with higher mortality. However, data in patients with end-stage renal disease are scarce. Therefore, we analyzed serum levels of sTNFR1 and sTNFR2 and investigated their association with inflammatory markers and mortality in dialysis patients.. RESEARCH DESIGN AND METHODS: This was a longitudinal cohort study of 207 prevalent patients (median age 66 years, 56% men) undergoing hemodialysis in Stockholm, Sweden. Demographics, clinical characteristics, including comorbidities and laboratory data, were obtained at baseline, together with prospective follow-up for mortality.. RESULTS: The median sTNFR1 and sTNFR2 levels were 17,680 ng/l [95% confidence interval (CI) 17,023-18,337] and 24,450 ng/l (95% CI 23,721-25,179), respectively. During a follow-up of 31 months (interquartile range, 21-38), 77 patients died. ...
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 ...
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 ...
Clone REA499 recognizes the human and mouse CD27 antigen, a single-pass type I membrane protein, also known as tumor necrosis factor receptor superfamily member 7 (TNFRSF7). CD27 is a member of the nerve growth factor receptor family and is exclusively expressed on cells of the lymphoid lineage, mostly in an activation-specific manner, and all enhance T cell receptor (TCR)-induced T cell expansion. CD27 and its ligand, CD70, have been defined at the protein, cDNA, and genomic level in both human and mouse. It is found on natural killer (NK), T, and B cell populations. In human and mice, the majority of CD4+ and CD8+ naive peripheral T cells express CD27 and expression is up-regulated upon TCR stimulation. Loss of CD27 expression is irreversible and seems to represent terminal effector T cell differentiation. In humans, naive B cells lack CD27 but antigen receptor stimulation induces expression. CD27+ B cells display all the functional and phenotypic characteristics of memory cells. Additional
Clone REAL173 is an antibody fragment derived from the full CD27 antibody molecule. It displays no binding to Fc receptors. The recombinantly engineered antibody fragments are multimerized to form the REAlease Complex to bind markers with high avidity. Clone REAL173 recognizes the human CD27 antigen, a single-pass type I membrane protein, also known as tumor necrosis factor receptor superfamily member 7 (TNFRSF7). CD27 is a member of the nerve growth factor receptor family and is exclusively expressed on cells of the lymphoid lineage, mostly in an activation-specific manner, and all enhance T cell receptor (TCR)-induced T cell expansion. CD27 and its ligand, CD70, have been defined at the protein, cDNA, and genomic level in both human and mouse. It is found on NK, T, and B cell populations. The majority of CD4+ and CD8+ naive peripheral T cells express CD27 and expression is up-regulated upon TCR stimulation. Loss of CD27 expression is irreversible and seems to represent terminal effector T cell
Somatic mutations of the tumor suppressor tumor necrosis factor receptor superfamily member 14 (HVEM, encoded by TNFRSF14), which frequently occur in follicular lymphomas (FL), disrupt the interaction between HVEM and the immune checkpoint protein B and T lymphocyte associated (BTLA), resulting in the inhibition of T-cell immune responses. To elucidate the role of HVEM in germinal center (GC) lymphomagenesis, Boice, Salloum, Mourcin, and colleagues evaluated the interaction between HVEM and BTLA in FLs. Genomic and immunohistochemical analyses of human FLs identified HVEM mutations in 28% (40 of 141) of patient samples and the mutually exclusive loss of either HVEM or BTLA expression in 73% (145 of 198) of patient samples. Depletion of B cell-specific Hvem or Btla in a genetically engineered mouse model of FL resulted in enhanced lymphomagenesis in Hvem-deficient mice and Btla-deficient mice compared to control mice. Further, the morphology and activated status of the B-cell receptor (BCR) ...
Damaged cells can die through different mechanisms. Two major forms of cell death are necrosis and apoptosis.1Apoptosis, also known as programmed cell death, is the form of cell elimination commonly occurring during development as well as in many physiologic and pathologic processes.2 3 In contrast, necrosis occurs mostly when noxious stimuli disintegrate the function of various cellular compartments leading to plasma membrane damage, mitochondrial dysfunction, and cell lysis.. The induction of the endogenous death machinery can be initiated via 2 principal signaling pathways.4 One involves the ligation of death receptors, such as CD95 and tumor necrosis factor-receptor (TNF-R1), which on binding of the adapter protein FADD, recruit procaspase-8 into the death-inducing signaling complex. Another pathway that is triggered by a number of apoptotic stimuli such as anticancer drugs or irradiation is essentially controlled at the mitochondrion. An initial event is the release of cytochrome c from ...
OBJECTIVE: We evaluated the full range effects of FOXO3a in endothelial cells (ECs) by microarray analysis and investigated the role of FOXO3a regulating TNF receptor signaling pathway. METHODS AND RESULTS: Human umbilical vein endothelial cells (HUVECs) were transfected with adenoviral vectors expressing constitutively active FOXO3a (Ad-TM-FOXO3a). Ad-TM-FOXO3a transfection caused remarkable apoptosis, which were accompanied with upregulation of genes related with TNF receptor signaling, such as TNF-alpha, TANK (TRAF-associated NF-kappaB activator), and TTRAP (TRAF and TNF receptor-associated protein). Furthermore, kappaB-Ras1 (IkappaB-interacting Ras-like protein-1) which is known to block IkappaB degradation was found increased, and intranuclear translocation of NF-kappaB was inhibited. GADD45beta and XIAP, negative regulators of c-Jun N-terminal kinase (JNK), were suppressed and JNK activity was increased. Attenuation of TNF signaling pathway either by blocking antibody for TNF receptor or ...
plasma membrane, receptor activity, positive regulation of I-kappaB kinase/NF-kappaB signaling, positive regulation of JNK cascade, tissue development
Full text for this publication is not currently held within this repository. Alternative links are provided below where available. ...
InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
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
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.
Monoclonal antibodies (mAbs) can be potent and highly specific therapeutics, diagnostics and research reagents. Nonetheless, mAb discovery using current in vivo or in vitro approaches can be costly and time-consuming, with no guarantee of success. We have established a platform for rapid discovery and optimization of mAbs ex vivo. This DTLacO platform derives from a chicken B cell line that has been engineered to enable rapid selection and seamless maturation of high affinity mAbs. We have validated the DTLacO platform by generation of high affinity and specific mAbs to five cell surface targets, the receptor tyrosine kinases VEGFR2 and TIE2, the glycoprotein TROP2, the small TNF receptor family member FN14, and the G protein-coupled receptor FZD10. mAb discovery is rapid and humanization is straightforward, establishing the utility of the DTLacO platform for identification of mAbs for therapeutic and other applications.
Pegah Khamehgir-Silz, Su-Hwan Kim (Research Training Group), Sebastian Lont, Cheryl Sultan, Andreas H. Wagner CD40 is a cell surface receptor belonging to the tumour necrosis factor receptor family. It is constitutively expressed by antigen-presenting cells such as monocyte/macrophages but also by non-immune cells like endothelial cells. The CD40 ligand (CD154), originally identified as a surface marker of activated T cells, is also present on activated platelets which release numerous bioactive mediators capable of modulating innate immune cells, activating endothelial cells, and influencing systemic immune responses. In endothelial cells, CD40-CD154 interaction causes a marked increase in the expression of pro-inflammatory adhesion molecules and chemokines which, in turn, promote the homing and extravasation of T cells, namely type 1 T-helper (Th1) cells, and monocyte/macrophages. In the vessel wall, Th1 cell differentiation and activity may additionally be controlled by natural T-regulatory ...
TRAF2 is an adaptor protein and ubiquitin ligase that is involved in mediating signals from the tumor necrosis factor receptors (TNFRs). Grech et al. investigated B cell signaling and proliferation in TRAF2-deficient mice. TRAF2-deficient B cells accumulated in conditionally deficient mice, leading to enlarged spleen and lymph nodes. Analysis of the TRAF2-deficient B cells showed that the processing of NF-κB2 p100 precursor into the cleaved p52 subunit was increased along with an increase in the DNA-binding activity of the p52 and RelB subunits, which indicates constitutive activation of the noncanonical NF-κB pathway. In addition, the cells were defective in activation of the canonical NF-κB pathway by antibodies that activate the TNFR family member, CD40, and did not show stimulation of proliferation, an increase in RelA activation, or phosphorylation and degradation of IκBα, the inhibitor of NF-κB, that occurs in wild-type cells. Processing of the NF-κB precursor was not further ...
This new study highlights the importance of certain soluble proteins, called cytokines, in Alzheimers disease. The study focuses on one of these cytokines, tumor necrosis factor-alpha(TNF), a critical component of the brains immune system. Normally, TNF finely regulates the transmission of neural impulses in the brain. The authors hypothesized that elevated levels of TNF in Alzheimers disease interfere with this regulation. To reduce elevated TNF, the authors gave patients an injection of an anti-TNF therapeutic called etanercept. Excess TNF-alpha has been documented in the cerebrospinal fluid of patients with Alzheimers. The new study documents a dramatic and unprecedented therapeutic effect in an Alzheimers patient: improvement within minutes following delivery of perispinal etanercept, which is etanercept given by injection in the spine. Etanercept (trade name Enbrel) binds and inactivates excess TNF. Etanercept is FDA approved to treat a number of immune-mediated disorders and is used ...
Complete information for TNFRSF1B gene (Protein Coding), TNF Receptor Superfamily Member 1B, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Complete information for TNFRSF8 gene (Protein Coding), TNF Receptor Superfamily Member 8, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Not knowable. I appreciate your concern, but this is the kind of data that cant be obtained by any means. Enbrel (etanercept) is an immunomodulator that may suppress the immune response which has a small impact on melanoma progress; its also given for psoriasis in which the skin cancer risk is already up. Its worth the risk; do keep a close eye on your skin so that skin cancers get rxd early & there s no risk of death ...
This noninferiority trial will investigate the tolerability and efficacy of two etanercept formulations (Reumatocept versus Enbrel) in patients with rheumatoid