1. Signaling Pathways
  2. NF-κB
  3. NF-κB

NF-κB (核因子κB)

Nuclear factor-κB; Nuclear factor-kappaB

NF-κB (Nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that controls transcription of DNA. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens. NF-κB plays a key role in regulating the immune response to infection. Incorrect regulation of NF-κB has been linked to cancer, inflammatory, and autoimmune diseases, septic shock, viral infection, and improper immune development. NF-κB has also been implicated in processes of synaptic plasticity and memory. There are five proteins in the mammalian NF-κB family: NF-κB1, NF-κB2, RelA, RelB, c-Rel.

目录号 产品名 作用方式 纯度
  • HY-18739
    Phorbol 12-myristate 13-acetate

    佛波酯

    Activator 99.66%
    Phorbol 12-myristate 13-acetate (PMA) 是一种佛波酯,是蛋白激酶 C (PKC)SphK 的激活剂。Phorbol 12-myristate 13-acetate 是 NF-κB 激活剂。Phorbol 12-myristate 13-acetate 可诱导 THP1 细胞分化。
  • HY-10227
    Bortezomib

    硼替佐米

    Inhibitor 99.97%
    Bortezomib (PS-341) 是一种可逆性和选择性的蛋白酶体 (proteasome) 抑制剂,通过靶向苏氨酸残基有效抑制 20S 蛋白酶体 (Ki=0.6 nM)。Bortezomib 破坏细胞周期、诱导细胞凋亡以及抑制核因子 NF-κB。Bortezomib 是第一种蛋白酶体抑制剂,具有抗癌活性。
  • HY-13453
    BAY 11-7082 Inhibitor 99.98%
    BAY 11-7082 (BAY 11-7821) 是一种 IκBα 磷酸化和 NF-κB 抑制剂,选择性且不可逆地抑制 TNF-α 诱导的 IκB-α 磷酸化,并减少 NF-κB 和粘附分子的表达。BAY 11-7082 抑制泛素特异性蛋白酶 USP7USP21 (IC50分别为 0.19, 0.96 μM)。BAY 11-7082 抑制脂质体中的 gasdermin D (GSDMD) 孔形成以及炎性体介导的细胞凋亡和人和小鼠细胞中IL-1β的分泌。
  • HY-100487
    TAK-243 Inhibitor 98.38%
    TAK-243 (MLN7243) 是一种首创的,选择性的泛素激活酶,UAE (UBA1) 抑制剂 (IC50=1 nM),其阻断了泛素结合,破坏了单泛素信号传导和全蛋白泛素化。TAK-243 (MLN7243) 诱导内质网应激 (ERS) 反应,消除 NF-κB 通路活化,促进细胞凋亡。
  • HY-13982
    JSH-23 Inhibitor 99.11%
    JSH-23 是 NF-κB 抑制剂,作用于脂多糖刺激的巨噬细胞 RAW 264.7,抑制 NF-κB 转录活性,IC50 为 7.1 μM。JSH-23 抑制 NF-κB p65 的核易位而不影响 IκBα 降解。
  • HY-W011474
    Geranylgeraniol

    香叶基香叶醇;基牻牛儿醇

    Inhibitor ≥98.0%
    Geranylgeraniol 是一种口服有效的维生素 K2 亚型,是甲戊酸途径 (mevalonate pathway) 的中间体。Geranylgeraniol 靶向 NF-kB 信号通路,可在动物模型中减轻脂多糖 (LPS) 诱导的小胶质细胞炎症。
  • HY-W016412
    Coenzyme Q0 Inhibitor ≥99.0%
    Coenzyme Q0 (CoQ0) 是一种口服有效的醌类化合物,可以从 Antrodia cinnamomea 中得到。Coenzyme Q0 诱导细胞凋亡 (apoptosis) 和自噬 (autophagy),抑制 HER-2/AKT/mTOR 信号通路来增强细胞凋亡和自噬机制。Coenzyme Q0 调节 NFκB/AP-1 的激活,并增强 Nrf2 的稳定,减轻炎症和氧化还原失衡。Coenzyme Q0 通过下调 MMP-9/NF-κB 和上调 HO-1 信号通路具有抗血管生成活性。
  • HY-147562
    ALPK1-IN-2 Inhibitor
    ALPK1-IN-2 (化合物 T001) 是一种有效的 ALPK1 (α- 激酶 1) 抑制剂,其 IC50 值为 95 nM。ALPK1-IN-2 还抑制 NF-κBIC50 值为 1.31 μM。
  • HY-18738
    Pyrrolidinedithiocarbamate ammonium

    吡咯烷二硫代氨基甲酸铵

    Inhibitor 99.04%
    Pyrrolidinedithiocarbamate ammonium (Ammonium pyrrolidinedithiocarbamate) 是选择性和具有血脑屏障通透性的 NF-κB 抑制剂。
  • HY-14655
    Sulfasalazine

    柳氮磺吡啶

    Inhibitor 99.10%
    Sulfasalazine (NSC 667219) 常用于类风湿关节炎和溃疡性结肠炎的相关演技。Sulfasalazine 可抑制 NF-κB 的活性。Sulfasalazine 是 type 1 的铁死亡 (ferroptosis) 诱导剂。
  • HY-N0822
    Shikonin

    紫草素

    Inhibitor 99.80%
    Shikonin 是中草药紫草的主要成分。Shikonin 是一种有效的 TMEM16A 氯化物通道 (chloride channel) 抑制剂,IC50 为 6.5 μM。Shikonin 是一种特异的丙酮酸激酶 M2 (PKM2) 抑制剂,还可以抑制 TNF-αNF-κB途径。Shikonin 通过抑制糖酵解降低外泌体 (exosome) 的分泌。Shikonin 抑制 AIM2炎性体活化。
  • HY-32735
    Triptolide

    雷公藤甲素

    Inhibitor 99.86%
    Triptolide是从雷公藤根中提取的二萜类三环氧化物,具有免疫抑制,抗炎,抗增殖和抗肿瘤作用。 雷公藤内酯是 NF-κB 活化的抑制剂。
  • HY-N0176
    Dihydroartemisinin

    双氢青蒿素

    Inhibitor 99.03%
    Dihydroartemisinin是一种有效的抗疟疾 (anti-malaria) 药物。
  • HY-14654
    Aspirin

    阿司匹林

    Inhibitor 99.66%
    Aspirin (Acetylsalicylic Acid) 是一种口服有效的不可逆的环氧合酶 COX-1COX-2 抑制剂,IC50 分别为 5 和 210 μg/mL. Aspirin 诱导细胞凋亡 (apoptosis)。Aspirin 可抑制 NF-κB 的活化。Aspirin 还抑制血小板前列腺素合成酶 (prostaglandin synthetase),可预防冠状动脉和脑血管血栓形成。
  • HY-N0197
    Baicalin

    黄芩苷

    Inhibitor 99.17%
    Baicalin 作为一种类黄酮糖苷,是一种变构肉碱棕榈酰转移酶1 (CPT1)是激活剂。Baicalin 降低 NF-κB 表达。
  • HY-10257
    BAY 11-7085 Inhibitor 99.99%
    BAY 11-7085 (BAY 11-7083) 是 NF-κB 激活和 IκBα 磷酸化的抑制剂,稳定 IκBα 的 IC50 值为 10 μM。
  • HY-19356
    Rocaglamide

    楝酰胺

    Inhibitor 99.34%
    Rocaglamide (Roc-A) 是从楝科植物中分离出来,可用于咳嗽,受伤,哮喘和炎症性皮肤病。Rocaglamide 是 T 细胞中一种有效的 NF-κB 活化抑制剂。Rocaglamide 是一种有效的选择性热休克因子 1 (HSF1) 活化抑制剂,IC50 约为 50 nM。Rocaglamide 还抑制翻译起始因子 eIF4A 的功能。Rocaglamide 还具有抗癌特性。
  • HY-N0141
    Parthenolide

    小白菊内酯

    Inhibitor 98.09%
    Parthenolide是在药草短舌匹菊中发现的倍半萜内酯。 Parthenolide通过抑制 NF-κB 活化而表现出抗炎活性; 它还可抑制 HDAC1 蛋白而不影响其他I/II类HDAC。
  • HY-10529
    Betulinic acid

    白桦脂酸

    Modulator ≥98.0%
    Betulinic acid 是一种天然的五环三萜类化合物,为真核细胞拓扑异构酶 I (topoisomerase I) 的抑制剂,IC50 值为 5 μM,具有抗炎,抗疟疾,抗艾滋病和抗肿瘤等活性。
  • HY-P0151
    SN50 Inhibitor 98.91%
    SN50是可渗透细胞的 NF-κB 易位抑制剂。

NF-κB transcription factors are critical regulators of immunity, stress responses, apoptosis and differentiation. In mammals, there are five members of the transcription factor NF-κB family: RELA (p65), RELB and c-REL, and the precursor proteins NF-κB1 (p105) and NF-κB2 (p100), which are processed into p50 and p52, respectively. NF-κB transcription factors bind as dimers to κB sites in promoters and enhancers of a variety of genes and induce or repress transcription. NF-κB activation occurs via two major signaling pathways: the canonical and the non-canonical NF-κB signaling pathways[1]

 

The canonical NF-κB pathway is triggered by signals from a large variety of immune receptors, such as TNFR, TLR, and IL-1R, which activate TAK1. TAK1 then activates IκB kinase (IKK) complex, composed of catalytic (IKKα and IKKβ) and regulatory (NEMO) subunits, via phosphorylation of IKKβ. Upon stimulation, the IKK complex, largely through IKKβ, phosphorylates members of the inhibitor of κB (IκB) family, such as IκBα and the IκB-like molecule p105, which sequester NF-κB members in the cytoplasm. IκBα associates with dimers of p50 and members of the REL family (RELA or c-REL), whereas p105 associates with p50 or REL (RELA or c-REL). Upon phosphorylation by IKK, IκBα and p105 are degradated in the proteasome, resulting in the nuclear translocation of canonical NF-κB family members, which bind to specific DNA elements, in the form of various dimeric complexes, including RELA-p50, c-REL-p50, and p50-p50. Atypical, IKK-independent pathways of NF-κB induction also provide mechanisms to integrate parallel signaling pathways to increase NF-κB activity, such as hypoxia, UV and genotoxic stress.

 

The non-canonical NF-κB pathway is induced by certain TNF superfamily members, such as CD40L, BAFF and lymphotoxin-β (LT-β), which stimulates the recruitment of TRAF2, TRAF3, cIAP1/2 to the receptor complex. Activated cIAP mediates K48 ubiquitylation and proteasomal degradation of TRAF3, resulting in stabilization and accumulation of the NFκB-inducing kinase (NIK). NIK phosphorylates and activates IKKα, which in turn phosphorylates p100, triggering p100 processing, and leading to the generation of p52 and the nuclear translocation of p52 and RELB[2][3].

 

Reference:

[1]. Oeckinghaus A, et al. The NF-kappaB family of transcription factors and its regulation.Cold Spring Harb Perspect Biol. 2009 Oct;1(4):a000034. 
[2]. Taniguchi K, et al. NF-κB, inflammation, immunity and cancer: coming of age. Nat Rev Immunol. 2018 May;18(5):309-324.
[3]. Perkins ND,et al. Integrating cell-signalling pathways with NF-kappaB and IKK function. Nat Rev Mol Cell Biol. 2007 Jan;8(1):49-62.

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