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-P99568
    Telitacicept
    		Inhibitor 99.30%
    Telitacicept (RC18) is a fully human TACI-Fc fusion protein. Telitacicept is a dual B lymphocyte stimulator (BLyS)/APRIL (a proliferation-inducing ligand) inhibitor that effectively blocks proliferation of B lymphocytes. Telitacicept can be used in research of B-cell autoimmune disease. The component ratio of this product is Active ingredient : Excipients = 1: 0.5-1: 0.8.
    Telitacicept
  • HY-133122
    UCB-9260
    		Inhibitor 99.36%
    UCB-9260, an orally active compound, inhibits TNF signaling by stabilising an asymmetric form of the trimer. UCB-9260 is selective for TNF over other superfamily members, and binds TNF with a similar Kd of 13 nM.
    UCB-9260
  • HY-N0029
    Forsythoside B
    		99.90%
    Forsythoside B is a phenylethanoid glycoside isolated from Forsythia suspensa (Thunb.) Vahl, a Chinese folk medicinal plant for treating inflammatory diseases and promoting blood circulation. Forsythoside B could inhibit TNF-alpha, IL-6, IκB and modulate NF-κB.
    Forsythoside B
  • HY-N0201
    Atractylenolide I
    		99.98%
    Atractylenolide I is a sesquiterpene derived from the rhizome of Atractylodes macrocephala, possesses diverse bioactivities, such as neuroprotective, anti-allergic, anti-inflammatory and anticancer properties. Atractylenolide I reduces protein levels of phosphorylated JAK2 and STAT3 in A375 cells, and acts as a TLR4-antagonizing agent.
    Atractylenolide I
  • HY-P99909
    Elranatamab
    		98.74%
    Elranatamab (PF-06863135) is an anti-CD3E/TNFRSF17 human IgG2κ monoclonal antibody. Recommend Isotype Controls: Human IgG2 kappa, Isotype Control (HY-P99002).
    Elranatamab
  • HY-P99056
    Utomilumab
    		Inhibitor 99.33%
    Utomilumab (PF 05082566) is a fully human IgG2 agonist monoclonal antibody that selectively binds to 4-1BB/CD137. Utomilumab can be used in the research of tumors such as follicular and other CD20+ non-Hodgkin lymphomas.
    Utomilumab
  • HY-111255
    SPD304
    		Inhibitor 99.72%
    SPD304 is a selective TNF-α inhibitor, which promotes dissociation of TNF trimers and therefore blocks the interaction of TNF and its receptor. SPD304 has an IC50 of 22 μM for inhibiting in vitro TNF receptor 1 (TNFR1) binding to TNF-α.
    SPD304
  • HY-P991028
    Surovatamig
    		99.89%
    Surovatamig (AZD0486; TNB-486) is a fully human anti-CD19/CD3 IgG4 bispecific antibody. Surovatamig triggers T cell activation, releases cytotoxic granules, and induces T cell-dependent cellular cytotoxicity and tumor cell lysis. Surovatamig can reduces release of pro-inflammatory cytokines including IL-2, IFNγ, TNF. Surovatamig can be used for the research of cancer, such as B cell non-Hodgkin lymphoma.
    Surovatamig
  • HY-N0405
    Orientin
    		Inhibitor 99.89%
    Orientin is a neuroprotective agentinhibits which has anti-inflammation, anti-oxidative, anti-tumor, and cardio protection properties. Orientin inhibits the levels of IL-6, IL-1β and TNF-α. Orientin increases IL-10 level. Orientin exhibits neuroprotective effect by inhibits TLR4 and NF-kappa B signaling pathway. Orientin can used in study neuropathic pain.
    Orientin
  • HY-N0722
    Neochlorogenic acid
    		Inhibitor 99.80%
    Neochlorogenic acid is a natural polyphenolic compound found in dried fruits and other plants. Neochlorogenic acid inhibits the production of TNF-α and IL-1β. Neochlorogenic acid suppresses iNOS and COX-2 protein expression. Neochlorogenic acid also inhibits phosphorylated NF-κB p65 and p38 MAPK activation.
    Neochlorogenic acid
  • HY-P99151
    Brentuximab
    		Inhibitor 99.64%
    Brentuximab (CAC-10) is a chimeric antibody targeting CD30. Brentuximab is conjugated with Monomethyl auristatin E (MMAE) (HY-15162) to form the antibody-drug conjugate Brentuximab vedotin (HY-P99107A). Brentuximab can be used for the research of cancer, such as lymphoma.
    Brentuximab
  • HY-P99111
    Golimumab
    		Inhibitor 99.77%
    Golimumab (CNTO-148) is a potent human IgG1 TNFα antagonist monoclonal antibody. Golimumab has anti-inflammation activitity and inhibits IL-6 and IL-1β production. Golimumab acts via targeting and neutralizing TNF to prevent inflammation and destruction of cartilage and bone. Golimumab has the anticancer activity and induces cell apoptosis. Golimumab can be used for rheumatoid arthritis, Crohn's disease and cancer research.
    Golimumab
  • HY-N0509
    Astilbin
    		Inhibitor 99.80%
    Astilbin is a flavonoid compound and enhances NRF2 activation. Astilbin also suppresses TNF-α expression and NF-κB activation.
    Astilbin
  • HY-107859
    Tris(2-chloroethyl) phosphate
    		Activator
    Tris(2-chloroethyl) phosphate (TCEP) is a widely used organic phosphorus flame retardant, mainly used as a plasticizer. Tris(2-chloroethyl) phosphate has orally active hepatotoxicity, inducing an increase in reactive oxygen species (ROS) and calcium ions (Ca²⁺) influx, a decrease in mitochondrial membrane potential (△Ψm), and causing DNA damage and cell apoptosis. Tris(2-chloroethyl) phosphate directly binds to FXR, inducing obesity and the formation of fatty liver in mice. Chloroethyl) phosphate activates the TLR4/NF-κB pathway, triggering liver inflammation.
    Tris(2-chloroethyl) phosphate
  • HY-P99653
    Ianalumab
    		Inhibitor 99.97%
    Ianalumab (VAY-736) is a human, decarboxylated antibody against BAFF-R. Ianalumab can block the interaction between BAFF and BAFF-R and antagonize the apoptosis protection mediated by BAFF. Ianalumab exerts antibody-dependent cytotoxic (ADCC), depending on effector cell activation mediated by immune receptor tyrosine activation motif (ITAM).
    Ianalumab
  • HY-N0297
    Sinensetin
    		Inhibitor 99.62%
    Sinensetin is a methylated flavonoid found in fruits that has strong anti-vascular and anti-inflammatory properties.
    Sinensetin
  • HY-P99796
    Ozoralizumab
    		Inhibitor 99.80%
    Ozoralizumab (ATN-103) is an anti-TNFα humanized antibody. Ozoralizumab is a humanized trivalent nanobody compound that consists of two anti-human TNFα nanobodies and an anti-human serum albumin (HSA) nanobody. Ozoralizumab can be used in research of arthritis.
    Ozoralizumab
  • HY-P990008
    Atrosab
    		Antagonist 99.94%
    Atrosab is a humanized IgG1 antagonistic anti-TNFR1 antibody. Atrosab inhibits TNF-mediated Apoptosis induction and IL-6 and IL-8 production. Atrosab reduces neurological deficits. Atrosab can be used for research of inflammatory disease. The recommend isotype control is Human IgG1 kappa, Isotype Control (HY-P99001).
    Atrosab
  • HY-P9970A
    Infliximab (Anti-TNF-α)
    		Inhibitor 99.00%
    Infliximab (Anti-TNF-α) (Avakine (Anti-TNF-α)) is a chimeric monoclonal IgG1 antibody that specifically binds to TNF-α. Infliximab (Anti-TNF-α) prevents the interaction of TNF-α with TNF-α receptor (TNFR1 and TNFR2). Infliximab (Anti-TNF-α) has the potential for autoimmune, chronic inflammatory diseases and diabetic neuropathy research.
    Infliximab (Anti-TNF-α)
  • HY-N0528
    Linarin
    		98.02%
    Linarin (Buddleoside) is an orally active and selective inhibitor of acetylcholinesterase (AChE). Linarin has many activities, such as anti-inflammatory, antioxidant, sleep aid and sedation, bone differentiation, anti-tumor, antibacterial and antiviral. Linarin can be used to study diseases such as the nervous system, osteoporosis and cancer.
    Linarin
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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