2. Signaling Pathways
  3. Apoptosis
  4. TNF Receptor

TNF Receptor

Tumor Necrosis Factor Receptor; TNFR

TNF Receptor

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Tumor necrosis factor (TNF) is a major mediator of apoptosis as well as inflammation and immunity, and it has been implicated in the pathogenesis of a wide spectrum of human diseases, including sepsis, diabetes, cancer, osteoporosis, multiple sclerosis, rheumatoid arthritis, and inflammatory bowel diseases.

TNF-α is a 17-kDa protein consisting of 157 amino acids that is a homotrimer in solution. In humans, the gene is mapped to chromosome 6. Its bioactivity is mainly regulated by soluble TNF-α–binding receptors. TNF-α is mainly produced by activated macrophages, T lymphocytes, and natural killer cells. Lower expression is known for a variety of other cells, including fibroblasts, smooth muscle cells, and tumor cells. In cells, TNF-α is synthesized as pro-TNF (26 kDa), which is membrane-bound and is released upon cleavage of its pro domain by TNF-converting enzyme (TACE).

Many of the TNF-induced cellular responses are mediated by either one of the two TNF receptors, TNF-R1 and TNF-R2, both of which belong to the TNF receptor super-family. In response to TNF treatment, the transcription factor NF-κB and MAP kinases, including ERK, p38 and JNK, are activated in most types of cells and, in some cases, apoptosis or necrosis could also be induced. However, induction of apoptosis or necrosis is mainly achieved through TNFR1, which is also known as a death receptor. Activation of the NF-κB and MAPKs plays an important role in the induction of many cytokines and immune-regulatory proteins and is pivotal for many inflammatory responses.

TNF Receptor Isoform Specific Products:

TNF Receptor Isoform Comparison
Cat. No. Product Name Effect Purity Chemical Structure
  • HY-N0182R
    Fisetin (Standard)
    		Inhibitor
    Fisetin (Standard) is the analytical standard of Fisetin. This product is intended for research and analytical applications. Fisetin is a natural flavonol found in many fruits and vegetables with various benefits, such as antioxidant, anticancer, neuroprotection effects.
    Fisetin (Standard)
  • HY-N6018
    β-Eudesmol
    		Activator 99.49%
    β-Eudesmol has anticancer and anti-inflammatory activities. Beta-Eudesmol can induce apoptosis. β-Eudesmol is a neostigmine antagonist. β-Eudesmol can antagonize neostigmine-induced neuromuscular failure. β-Eudesmoll can be used in the study of sepsis diseases. β-Eudesmol is a sesquiterpene-like compound that can be extracted from the rhizome of Atractylodes lancea.
    β-Eudesmol
  • HY-150725C
    ODN 1585 sodium
    		Inducer
    ODN 1585 sodium is a potent inducer of IFN and TNFα production. ODN 1585 sodium is a potent stimulator of NK (natural killer) function. ODN 1585 sodium increases CD8+ T-cell function, including the CD8+ T cell-mediated production of IFN-γ. ODN 1585 sodium induces regression of established melanomas in mice. ODN 1585 sodium can confer complete protection against malaria in mice. ODN 1585 sodium can be used for acute myelogenous leukemia (AML) and malaria research. ODN 1585 sodium can be used as a vaccine adjuvant.
    ODN 1585 sodium
  • HY-10406
    Talmapimod
    		Inhibitor 98.68%
    Talmapimod (SCIO-469) is an orally active and selective inhibitor of p38α MAPK with an IC50 of 9 nM. Talmapimod inhibits the secretion of inflammatory factors (such as TNFα, IL-1β, IL-6, and VEGF) by suppressing the p38α MAPK pathway, and it also inhibits angiogenesis and osteoclast activation. Talmapimod inhibits the growth of multiple myeloma cells and induces apoptosis. Talmapimod can be used to study various hematological malignancies (such as multiple myeloma, myelodysplastic syndrome).
    Talmapimod
  • HY-P99742
    Mitazalimab
    		Inhibitor 99.23%
    Mitazalimab (ADC-1013; JNJ-64457107) is FcγR-dependent CD40 agonist with tumor-directed activity. Mitazalimab activates antigen-presenting cells, e.g. dendritic cells (DC), to initiate tumor-reactive T cells. Therefore, Mitazalimab induces tumor-specific T cells to infiltrate and kill tumors. Mitazalimab remodels the tumor-infiltrating myeloid microenvironment.
    Mitazalimab
  • HY-30235A
    Benzydamine hydrochloride
    		Inhibitor 99.21%
    Benzydamine hydrochloride is an orally administered prostaglandin synthesis inhibitor that has anti-inflammatory, analgesic, antipyretic, and antibacterial properties. Benzydamine hydrochloride can inhibit TNF-α, stabilize cell membranes, and reduce oxidative stress within cells.
    Benzydamine hydrochloride
  • HY-110247
    TRAF-STOP inhibitor 6877002
    		Inhibitor 99.67%
    TRAF-STOP inhibitor 6877002 is a selective CD40-TRAF6 interaction inhibitor. TRAF-STOP inhibitor 6877002 exerts anti-atherosclerotic activity by blocking the CD40-TRAF6 signaling pathway, inhibiting classical monocyte activation, leukocyte recruitment, and macrophage activation and migration. TRAF-STOP inhibitor 6877002 reduces the phosphorylation levels of signaling intermediates in the canonical NF-κB pathway.
    TRAF-STOP inhibitor 6877002
  • HY-N0635
    Prim-O-glucosylcimifugin
    		99.87%
    Prim-O-glucosylcimifugin exerts anti-inflammatory effects through the inhibition of iNOS and COX-2 expression by through regulating JAK2/STAT3 signaling.
    Prim-O-glucosylcimifugin
  • HY-Y0399
    L-Norvaline
    		Antagonist ≥98.0%
    L-Norvaline is the inhibitor for arginase, that promotes the production of NO, reduces oxidative stress, improves insulin resistance, and exhibits antioxidant and anti-hyperglycemic effects. L-Norvaline can be used in research of Alzheimer’s disease.
    L-Norvaline
  • HY-N9965
    2'-Fucosyllactose
    		Inhibitor 99.97%
    2'-Fucosyllactose (2'-FL) is an oligosaccharide that could be derived from human milk. 2'-Fucosyllactose regulates the expression of CD14, alleviates colitis and regulates the gut microbiome. 2'-Fucosyllactose stimulates T cells to increase IFN-γ production and decreases IL-6, IL-17, and TNF-α production of cytokines.
    2'-Fucosyllactose
  • HY-P990794
    Anti-Mouse TNF-alpha/TNFSF2 Antibody (XT3.11)
    		Inhibitor 98.19%
    Anti-Mouse TNF-alpha/TNFSF2 Antibody (XT3.11) is a rat-derived IgG1 antibody inhibitor, targeting to TNF-alpha/TNFSF2. Anti-Mouse TNF-alpha/TNFSF2 Antibody (XT3.11) neutralizes of TNF-alpha. Anti-Mouse TNF-alpha/TNFSF2 Antibody (XT3.11) can be used for the researches of cancer, infection and immunology, such as dengue virus and B16K1 tumor.
    Anti-Mouse TNF-alpha/TNFSF2 Antibody (XT3.11)
  • HY-N0481
    Roburic acid
    		Inhibitor 99.93%
    Roburic acid acts as an anti-inflammatory, anti-tumor and osteoclastogenesis inhibitor, with a Ki of 7.066 μM against human TNF, an IC50 of 9 μM against human COX-2, and an IC50 of 5 μM against ovine COX-1. Roburic acid reduces the production of inflammatory mediators such as NO and IL-6 in macrophages by inhibiting the NF-κB and MAPK (p38/JNK) pathways. By competitively inhibiting the TNF-TNF-R1 interaction, Roburic acid blocks the downstream NF-κB signaling pathway, thereby inducing cell cycle arrest and apoptosis in cancer cells. Roburic acid specifically inhibits osteoclastogenesis and bone resorption by suppressing the RANKL/TRAF6/NF-κB/NFATc1 axis. Roburic acid can be used in research related to osteolytic diseases such as osteoporosis, colorectal cancer and inflammatory diseases.
    Roburic acid
  • HY-P990070
    Zigakibart
    		Inhibitor 99.30%
    Zigakibart (BION-1301) is an IgG4-kappa, humanized monoclonal antibody against TNFSF13 (tumor necrosis factor (TNF) superfamily member 13, APRIL, CD256). Zigakibart exhibits anti-inflammatory activity.
    Zigakibart
  • HY-150725
    ODN 1585
    		Inducer
    ODN 1585 is a potent inducer of IFN and TNFα production. ODN 1585 is a potent stimulator of NK (natural killer) function. ODN 1585 increases CD8+ T-cell function, including the CD8+ T cell-mediated production of IFN-γ. ODN 1585 induces regression of established melanomas in mice. ODN 1585 can confer complete protection against malaria in mice. ODN 1585 can be used for acute myelogenous leukemia (AML) and malaria research. ODN 1585 can be used as a vaccine adjuvant.
    ODN 1585
  • HY-P99459
    Baminercept
    		99.97%
    Baminercept (BG 9924; TT-47) is an Ig fusion protein targeting the lymphotoxin β receptor (LTβR). Baminercept effectively regulates subsets of circulating immune cells by inhibiting LIGHT, LT-α1β2 and their receptors. Baminercept also increases blood lymphocyte counts and reduces plasma CXCL13 levels. Baminercept carries a high risk of hepatotoxicity. Baminercept can be used in research on rheumatoid arthritis and primary Sjögren's syndrome.
    Baminercept
  • HY-W011404
    Tributyrin
    		Inhibitor 98.91%
    Tributyrin (Glyceryl tributyrate), a neutral short-chain fatty acid triglyceride, is a stable and rapidly absorbed proagent of Butyric Acid. Tributyrin diffuses through biological membranes and is metabolized by intracellular lipases, releasing effective butyrate directly into the cell in vivo. Tributyrin has potent antiproliferative, proapoptotic and differentiation-inducing effects.
    Tributyrin
  • HY-N2468
    Xylobiose
    		98.0%
    Xylobiose (1,4-β-D-Xylobiose; 1,4-D-Xylobiose) is an orally active Claudin 2/CLDN2 inhibitor and HSP27 inducer. Xylobiose works by regulating intestinal barrier function and glucose and lipid metabolism-related signaling pathways. Xylobiose inhibits CLDN2 expression to reduce intestinal permeability, induces HSP27 to enhance cell protection, and regulates the miR-122a/miR-33a axis to inhibit liver lipid synthesis and improve insulin resistance. Xylobiose can strengthen intestinal barrier integrity, reduce blood sugar and blood lipid levels, and reduce oxidative stress and inflammatory response. Xylobiose can be used in the study of type 2 diabetes and metabolic syndrome.
    Xylobiose
  • HY-P99670
    Iscalimab
    		Inhibitor 99.64%
    Iscalimab (CFZ-533) is a non-depleting IGg1 monoclonal antibody targeting CD40 (KD: 0.3 nM). Iscalimab can be used for research of Graves' hyperthyroidism and autoimmune diseases.
    Iscalimab
  • HY-N0152
    Myricitrin
    		Inhibitor 99.76%
    Myricitrin, a naturally occurring flavonoid, is an orally active nitric oxide (NO) and PKC inhibitor. Myricitrin has central nervous system activity, including anxiolytic-like action. Myricitrin possesses antioxidant, anti-inflammatory, antifibrotic and anti-malarial effects.
    Myricitrin
  • HY-N2119
    Sciadopitysin
    		99.0%
    Sciadopitysin is a type of biflavonoids in leaves from ginkgo biloba. Sciadopitysi inhibits RANKL-induced osteoclastogenesis and bone loss by inhibiting NF-κB activation and reducing the expression of c-Fos and NFATc1.
    Sciadopitysin
Cat. No. Product Name / Synonyms Species Source
Cat. No. Product Name / Synonyms Application Reactivity
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Download TNF Receptor Signaling Pathway Map.

Following the binding of TNF to TNF receptors, TNFR1 binds to TRADD, which recruits RIPK1, TRAF2/5 and cIAP1/2 to form TNFR1 signaling complex I; TNFR2 binds to TRAF1/2 directly to recruit cIAP1/2. Both cIAP1 and cIAP2 are E3 ubiquitin ligases that add K63 linked polyubiquitin chains to RIPK1 and other components of the signaling complex. The ubiquitin ligase activity of the cIAPs is needed to recruit the LUBAC, which adds M1 linked linear polyubiquitin chains to RIPK1. K63 polyubiquitylated RIPK1 recruits TAB2, TAB3 and TAK1, which activate signaling mediated by JNK and p38, as well as the IκB kinase complex. The IKK complex then activates NF-κB signaling, which leads to the transcription of anti-apoptotic factors-such as FLIP and Bcl-XL-that promote cell survival. 

 

The formation of TNFR1 complex IIa and complex IIb depends on non-ubiquitylated RIPK1. For the formation of complex IIa, ubiquitylated RIPK1 in complex I is deubiquitylated by CYLD. This deubiquitylated RIPK1 dissociates from the membrane-bound complex and moves into the cytosol, where it interacts with TRADD, FADD, Pro-caspase 8 and FLIPL to form complex IIa. By contrast, complex IIb is formed when the RIPK1 in complex I is not ubiquitylated owing to conditions that have resulted in the depletion of cIAPs, which normally ubiquitylate RIPK1. This non-ubiquitylated RIPK1 dissociates from complex I, moves into the cytosol, and assembles with FADD, Pro-caspase 8, FLIPL and RIPK3 (but not TRADD) to form complex IIb. For either complex IIa or complex IIb to prevent necroptosis, both RIPK1 and RIPK3 must be inactivated by the cleavage activity of the Pro-caspase 8-FLIPL heterodimer or fully activated caspase 8. The Pro-caspase 8 homodimer generates active Caspase 8, which is released from complex IIa and complex IIb. This active Caspase 8 then carries out cleavage reactions to activate downstream executioner caspases and thus induce classical apoptosis. 

 

Formation of the complex IIc (necrosome) is initiated either by RIPK1 deubiquitylation mediated by CYLD or by RIPK1 non-ubiquitylation due to depletion of cIAPs, similar to complex IIa and complex IIb formation. RIPK1 recruits numerous RIPK3 molecules. They come together to form amyloid microfilaments called necrosomes. Activated RIPK3 phosphorylates and recruits MLKL, eventually leading to the formation of a supramolecular protein complex at the plasma membrane and necroptosis [1][2].

 

Reference:
[1]. Brenner D, et al. Regulation of tumour necrosis factor signalling: live or let die.Nat Rev Immunol. 2015 Jun;15(6):362-74. 
[2]. Conrad M, et al. Regulated necrosis: disease relevance and therapeutic opportunities.Nat Rev Drug Discov. 2016 May;15(5):348-66. 
 

TNF Receptor Isoform Comparison

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