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-113763
    TWEAK-Fn14-IN-1
    		Inhibitor 99.62%
    TWEAK-Fn14-IN-1 (Compound L524-0366) is a specific dose-dependent TWEAK-Fn14 inhibitor. TWEAK-Fn14-IN-1 binds specifically to the Fn14 surface with a KD of 7.12 μM. TWEAK-Fn14-IN-1 inhibits TWEAK induced glioma cell migration without any potential cytotoxic effects.
    TWEAK-Fn14-IN-1
  • HY-N8593
    Undecane
    		Inhibitor 99.66%
    Undecane is a potent cAMP agonist with anti-allergic and anti-inflammatory activities. Undecane inhibits degranulation and the secretion of histamine and TNF-α. Undecane reverses the increased levels of p38 phosphorylation, NF-κB transcriptional activity and target cytokine/chemokine genes, including thymus and activation-regulated chemokine (TARC), macrophage-derived chemokine (MDC) and interleukin-8 (IL-8). Undecane can be used for the study of skin inflammatory disorders, such as atopic dermatitis.
    Undecane
  • HY-138793
    2-(2,6-Dioxopiperidin-3-yl)phthalimidine
    		Inhibitor 99.67%
    2-(2,6-Dioxopiperidin-3-yl)phthalimidine (EM-12), a teratogenic Thalidomide analogue, is more active than Thalidomide and is much more stable for hydrolysis. 2-(2,6-Dioxopiperidin-3-yl)phthalimidine enhances 1,2-dimethylhydrazine-induction of rat colon adenocarcinomas.
    2-(2,6-Dioxopiperidin-3-yl)phthalimidine
  • HY-W753791
    (±)-Perillaldehyde
    		Inhibitor
    (±)-Perillaldehyde has an antidepressant effect by modulating the olfactory nervous system in a mouse model of stress-induced depression. (±)-Perillaldehyde also has anti-inflammatory activity, inducing JNK activation in RAW264.7 cells and inhibiting the expression of TNF-α, with an IC50 of 171.7 μM.
    (±)-Perillaldehyde
  • HY-P990124
    Anti-Mouse GITR Antibody (DTA-1)
    		Agonist 98.47%
    Anti-Mouse GITR Antibody (DTA-1) is a rat derived IgG2b monoclonal agonist antibody targeting mouse GITR. Anti-Mouse GITR Antibody (DTA-1) can activate T cells and B cells to enhance immune response. Anti-Mouse GITR Antibody (DTA-1) selectively enhances Th2 cell effector function through GITR signaling. Anti-Mouse GITR Antibody (DTA-1) may exacerbate allergic reactions. Anti-Mouse GITR Antibody (DTA-1) can be used for researches on cancer and allergic conditions such as colon cancer and allergic asthma. The recommed isotype control of Anti-Mouse GITR Antibody (DTA-1) is Rat IgG2b kappa, Isotype Control (HY-P990682).
    Anti-Mouse GITR Antibody (DTA-1)
  • HY-100573A
    (E/Z)-Necrosulfonamide
    		Inhibitor 98.84%
    (E/Z)-Necrosulfonamide is a racemic compound of Necrosulfonamide (HY-100573). Necrosulfonamide is a MLKL and Gasdermin D (GSDMD) inhibitor, capable of separately inhibiting necroptosis and pyroptosis of cells. Necrosulfonamide does not affect the activation of upstream signals, but specifically inhibits the downstream executor oligomerization step. Necrosulfonamide reduces the expression of the key kinases NLRP3 and caspase-1 involved in necroptosis and pyroptosis, activate the Nrf2 pathway and the downstream antioxidant enzymes, and also downregulates a variety of inflammatory factors. Necrosulfonamide plays significant roles in various diseases such as neurodegenerative diseases (such as Parkinson’s disease), tissue damage and ischemia-reperfusion injury, inflammatory bowel disease, osteoarthritis and fracture repair, and hair loss by regulating two important programmed necrosis pathways.
    (E/Z)-Necrosulfonamide
  • HY-P99015
    Dacetuzumab
    		Inhibitor
    Dacetuzumab (SGN-40) is a humanized IgG1, anti-CD40 monoclonal antibody with anti-lymphoma activity. Dacetuzumab kills tumor cells via immune effector functions (antibody-dependent cellular cytotoxicity and phagocytosis [ADCC/ADCP]). Dacetuzumab ((SGN-40) can be used for multiple myeloma research.
    Dacetuzumab
  • HY-P990040
    Exlinkibart
    		Inhibitor 99.66%
    Exlinkibart (LVGN-6051) targets TNFRSF9 and is an IgG1κ antibody humanized through complementarity-determining region (CDR) grafting technology.
    Exlinkibart
  • HY-P99321
    Teneliximab
    		Inhibitor ≥99.0%
    Teneliximab (BMS-224819) is a chimeric monoclonal antibody, blocks the CD40-CD40L interaction. Teneliximab (BMS-224819) has partial agonist activity resulting in some signaling through CD40 and peripheral B cell depletion.
    Teneliximab
  • HY-N6580
    Ginsenoside Rg4
    		Inhibitor 99.94%
    Ginsenoside Rg4 is an orally active protopanaxatriol type ginsenoside. Ginsenoside Rg4 can activate PI3K, AKT and GSK-3β signaling. Ginsenoside Rg4 can inhibit ROS and inflammatory cytokine levels. Ginsenoside Rg4 can be used for the researches of inflammation, infection and metabolic disease, such as sepsis and lung inflammation.
    Ginsenoside Rg4
  • HY-N0262R
    Cordycepin (Standard)
    Cordycepin (Standard) is the analytical standard of Cordycepin. This product is intended for research and analytical applications. Cordycepin (3'-Deoxyadenosine) is a nucleoside derivative and inhibits IL-1β-induced MMP-1 and MMP-3 expression in rheumatoid arthritis synovial fibroblasts (RASFs) in a dose-dependent manner. Cordycepin kills Mycobacterium tuberculosis through hijacking the bacterial adenosine kinase.
    Cordycepin (Standard)
  • HY-P99669
    Iratumumab
    		Inhibitor 98.95%
    Iratumumab (MDX-060) a human anti-CD30 IgG1κ monoclonal antibody. Iratumumab inhibits the growth of CD30-expressing tumor cells. Iratumumab can be used for research of Hodgkin's lymphoma (HL) and anaplastic large-cell lymphoma (ALCL).
    Iratumumab
  • HY-101170
    BU224 hydrochloride
    		Inhibitor
    BU224 hydrochloride is a selective and high affinity imidazoline I2 receptor ligand, with a Ki of 2.1 nM. BU224 hydrochloride is sometimes used as an I2 receptor antagonist. BU224 hydrochloride exerts neuroprotective effects, with anti-inflammatory and anti-apoptotic properties. BU224 hydrochloride improves memory in 5XFAD mice, enlarging dendritic spines and reducing Aβ-induced changes in NMDARs. BU224 hydrochloride can be used for Alzheimer's disease research.
    BU224 hydrochloride
  • HY-164102
    TNF-α-IN-18
    		Inhibitor 98.94%
    TNF-α-IN-18 (Compound 61) is an inhibitor for TNF-α (IC50 of 1.8 μM), that inhibits TNF signaling pathway through block of NF-kB migration from cytoplasm to nucleus. TNF-α-IN-18 exhibits slight cytotoxicity to mouse fibroblast LM cell, with a CC50 >50 μM. TNF-α-IN-18 ameliorates the TNF- or Lipopolysaccharide (HY-D1056)-induced sepsis in mouse models. TNF-α-IN-18 protects mice from rheumatoid arthritis.
    TNF-α-IN-18
  • HY-N8435
    Desoxo-narchinol A
    		Inhibitor 98.0%
    Desoxo-narchinol A is an orally active and potent anti-inflammatory agent. Desoxo-narchinol A can be isolated from the roots and rhizomes of Nardostachys jatamansi. Desoxo-narchinol A can be used for septic shock and inflammatory diseases research.
    Desoxo-narchinol A
  • HY-15790H
    (S)-Elobixibat
    		Inhibitor 98.75%
    (S)-Elobixibat is the S enantiomer of Elobixibat (HY-15790). (S)-Elobixibat is an orally effective Apical Sodium-Dependent Bile (IBAT) inhibitor. (S)-Elobixibat decreases LDL cholesterol, increases serum GLP-1, promotes colon motility, and has the potential to treat metabolic syndrome. (S)-Elobixibat can be used to study constipation, dyslipidemia, non-alcoholic hepatitis, and liver tumors.
    (S)-Elobixibat
  • HY-P1875A
    TNF-α (46-65), human TFA
    		99.90%
    TNF-α (46-65), human (TFA) is a peptide of human TNF-α.
    TNF-α (46-65), human TFA
  • HY-P99775
    Placulumab
    		Inhibitor
    Placulumab (ART621) is an anti-TNF α monoclonal antibody. Placulumab has anti-inflammatory activity and has potential applications in inflammatory diseases such as arthritis.
    Placulumab
  • HY-P10551
    ApoA-I mimetic peptide 5A
    		Inhibitor
    ApoA-I mimetic peptide 5A is a synthetic peptide molecule designed based on the structure and function of naturally occurring apolipoprotein A-I (Apo A-I). ApoA-I mimetic peptide 5A can promote the efflux of cholesterol from cells and help reduce the accumulation of cholesterol in cells. ApoA-I mimetic peptide 5A also shows anti-inflammatory activity and can reduce inflammatory markers in blood and tissues. ApoA-I mimetic peptide 5A can be used in the study of cardiovascular diseases.
    ApoA-I mimetic peptide 5A
  • HY-N3595
    Cleomiscosin A
    		Inhibitor 99.15%
    Cleomiscosin A is a coumarino-lignoid from branch of Macaranga adenantha. Cleomiscosin A is active against TNF-alpha secretion of the mouse peritoneal macrophages.
    Cleomiscosin A
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. 
 

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