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    1. Apoptosis
    2. TNF Receptor

    TNF Receptor

    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.

    View TNF Receptor Pathway Map

    TNF Receptor 相关产品 (45):

    Cat. No. Product Name Effect Purity
    • HY-A0003
      Lenalidomide Inhibitor 99.98%
      Lenalidomide是用作免疫调节药物的 TNF-α 抑制剂。它还具有抗血管生成活性。
    • HY-16046
      Rimiducid Activator 99.05%
      Rimiducid (AP1903) 是二聚化剂,其通过交联 FKBP 结构域起作用,启动 Fas 信号传导,引起凋亡
    • HY-10984
      Pomalidomide Inhibitor 99.86%
      Pomalidomide是一种抗血管生成剂和免疫调节剂。 Pomalidomide在LPS刺激的人PBMC中抑制 TNF-α 释放,IC50 为13 nM。
    • HY-N0822
      Shikonin Inhibitor 99.64%
      Shikonin是中草药紫草的主要成分。 Shikonin显示出各种生物活性,包括抑制TNF-αNF-κBHIV-1
    • HY-13812
      QNZ Inhibitor 98.46%
      QNZ 强抑制 NF-κB 转录激活和 TNF-α 产生,IC50 分别为 11 和 7 nM。QNZ 是一种保护神经的钙池操纵的钙通道 (SOC) 抑制剂。
    • HY-108847
      Etanercept Inhibitor
      Etanercept (Enbrel) 是一种肿瘤坏死因子(TNF),用于治疗类风湿性关节炎,强直性脊柱炎,银屑病关节炎和斑块状银屑病。
    • HY-111255
      SPD304 Inhibitor >99.0%
      SPD304是肿瘤坏死因子α (TNFα) 的选择性抑制剂,能够促进肿瘤坏死因子三聚体的分离,从而阻断其与受体间的相互作用,其体外抑制肿瘤坏死因子α和受体1间结合的IC50 值为22 μM。SPD304毒性高,不能用于体内。
    • HY-N0472
      Geraniin Inhibitor
      Geraniin 是具有抗肿瘤、抗炎、抗高血糖活性的、肿瘤坏死因子α (TNF-α) 的释放抑制剂,其 IC50 值为 43 μM。
    • HY-15615A
      TIC10 Agonist 99.68%
      TIC10是一种有效,有口服活性,稳定的 TRAIL 诱导剂,其通过抑制 AktERK 起作用,从而激活Foxo3a并显着诱导细胞表面TRAIL。
    • HY-N0182
      Fisetin Inhibitor 98.02%
    • HY-P0224
      N-Formyl-Met-Leu-Phe Inhibitor 99.46%
      N-Formyl-Met-Leu-Phe (fMLP; N-Formyl-MLF) 是一种趋化肽和N-甲酰基肽受体 (FPR) 的特异性配体。报道显示N-Formyl-Met-Leu-Ph 可抑制 TNF-alpha 的分泌。
    • HY-A0003B
      Lenalidomide hemihydrate Inhibitor 99.82%
      Lenalidomide是沙利度胺类似物,其抑制肿瘤血管生成,肿瘤增殖和肿瘤分泌细胞因子,包括TNF-αIL 6
    • HY-32018
      Cot inhibitor-2 Inhibitor 99.20%
      Cot 抑制剂-2是COT/Tpl2抑制剂。
    • HY-N2027
      Taurochenodeoxycholic acid Inhibitor 99.80%
      Taurochenodeoxycholic acid是动物胆汁酸的主要生物活性物质之一。
    • HY-14622
      Necrostatin 2 Inhibitor 99.97%
      Necrostatin 2 是一种有效的程序性坏死 (necroptosis) 抑制剂。作用于TNF-α处理的FADD缺陷型Jurkat T细胞,抑制程序性坏死,EC50 为 0.05 μM。
    • HY-14622A
      Necrostatin 2 racemate Inhibitor 99.10%
      Necrostatin 2是高活性的坏死性凋亡抑制剂,EC50为50nM。
    • HY-P9908
      Adalimumab Inhibitor 98.12%
      Adalimumab 是一种人源的单克隆 IgG1 抗体,靶向肿瘤坏死因子α (TNF-α)。
    • HY-100735
      C 87 Inhibitor >98.0%
      C87是一种新型小分子TNFα抑制剂; 高效抑制TNFα诱导的细胞毒性,IC50值为8.73 μM。
    • HY-N0297
      Sinensetin Inhibitor 99.22%
    • HY-N0029
      Forsythoside B 99.99%
      Forsythoside B是传统中药植物独一味的叶子中分离的苯乙醇苷。独一味可用于治疗炎症疾病和促进血液循环。Forsythoside B 可抑制 TNF-alphaIL-6IκB, 调节 NF-κB

    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].


    [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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