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

NF-κB (核因子κB)

Nuclear factor-κB; Nuclear factor-kappaB

NF-κB(活化 B 细胞的核因子 κ 轻链增强子)是一种控制 DNA 转录的蛋白质复合物。NF-κB 存在于几乎所有动物细胞类型中,并参与细胞对压力、细胞因子、自由基、紫外线照射、氧化 LDL 以及细菌或病毒抗原等刺激的反应。NF-κB 在调节对感染的免疫反应中起着关键作用。NF-κB 的错误调节与癌症、炎症和自身免疫性疾病、感染性休克、病毒感染和免疫发育不当有关。NF-κB 还与突触可塑性和记忆过程有关。哺乳动物 NF-κB 家族中有五种蛋白质:NF-κB1、NF-κB2、RelA、RelB、c-Rel。

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.

Cat. No. Product Name Effect Purity Chemical Structure
  • HY-18739
    Phorbol 12-myristate 13-acetate

    佛波酯

    Activator 99.80%
    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 THP-1 细胞分化 (已经经过 MCE 专业的生物实验验证)。
    Phorbol 12-myristate 13-acetate
  • 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。
    Bortezomib
  • 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。
    BAY 11-7082
  • 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。
    TAK-243
  • HY-13982
    JSH-23 Inhibitor 99.92%
    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。
    JSH-23
  • HY-173063
    TLR8 antagonist-1 Inhibitor 99.95%
    TLR8 antagonist-1 (Compound 10) 是一种选择性 TLR8 拮抗剂。TLR8 antagonist-1 可抑制 TLR8 介导的炎症和信号通路,减少 MyD88 募集以及抑制 NF-κBIRF 通路。TLR8 antagonist-1 具有抗炎的活性。
    TLR8 antagonist-1
  • HY-W015883S1
    Fumaric acid-13C2
    Fumaric acid-13C213C 标记的 Fumaric acid (HY-W015883)。Fumaric acid 是一种不饱和二碳酸,是柠檬酸循环的中间产物,以 ATP 的形式为细胞内提供能量。Fumaric acid 通过抑制依赖 p38 MAPK 的 NF-κB 信号通路发挥抗炎作用。Fumaric acid 可用于妊娠高血压的研究。
    Fumaric acid-<sup>13</sup>C<sub>2</sub>
  • HY-171658
    R1-ICR-5 Activator
    R1-ICR-5 是一种选择性的靶向丝氨酸/苏氨酸蛋白激酶 1 (RIPK1) PROTAC 降解剂。R1-ICR-5 通过 VHL 介导,促使 RIPK1 发生降解,进而失调 TNFR1 和 TLR3/4 信号枢纽,增强 NF-κB、MAPK 和 IFN 信号输出,同时促进 RIPK3 激活和坏死性凋亡的诱导。R1-ICR-5 有望用于癌症和炎症性疾病的研究。(粉色:PK68 (HY-128348);黑色:linker (HY-W012241);蓝色:(S,R,S)-AHPC (HY-125845)。
    R1-ICR-5
  • HY-14654
    Aspirin

    阿司匹林

    Inhibitor 99.90%
    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。
    Aspirin
  • 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。
    Triptolide
  • 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。
    Shikonin
  • HY-N0197
    Baicalin

    黄芩苷

    Inhibitor 98.92%
    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) 的激活剂。Baicalin 降低 NF-κB 表达。
    Baicalin
  • HY-15027
    5-Aminosalicylic Acid

    5-氨基水杨酸

    Inhibitor 99.97%
    5-Aminosalicylic acid (Mesalamine) 是一种特异性的 PPARγ 激动剂,还抑制 p21-激活激酶1 (PAK1) 和 NF-κB。5-Aminosalicylic acid 可抑制骨桥蛋白 (OPN) 的活性。
    5-Aminosalicylic Acid
  • HY-14655
    Sulfasalazine

    柳氮磺吡啶

    Inhibitor 99.04%
    Sulfasalazine (NSC 667219) 常用于类风湿关节炎和溃疡性结肠炎的相关研究。Sulfasalazine 可抑制 NF-κB 的活性。Sulfasalazine 是 type 1 的铁死亡 (ferroptosis) 诱导剂。
    Sulfasalazine
  • HY-B1449
    Uridine

    尿苷

    Inhibitor 99.98%
    Uridine (β-Uridine) 是一种核苷化合物, 由尿嘧啶与核糖环组成, 两者由β-N1-配糖键相连。
    Uridine
  • HY-N0171A
    Beta-Sitosterol (purity>98%)

    β-谷甾醇 (purity>98%)

    Inhibitor 99.74%
    Beta-Sitosterol (purity>98%) 具有口服活性。Beta-Sitosterol 具有抗炎、抗癌、抗氧化、抗菌、抗糖尿病、抗氧化酶、镇痛等多种活性。Beta-Sitosterol 通过降低 ROSTNF-αIL-1βNF-κB p65 的水平以及恢复 HIF-1α/mTOR 信号通路活力来抑制牛乳腺上皮细胞炎症和脂肪生成障碍。Beta-Sitosterol 通过 ROS 介导的线粒体失调和 p53 激活诱导癌细胞凋亡 (apoptosis)。Beta-Sitosterol 在癌细胞中通过激活 caspase-3caspase-8caspase-9,介导 PARP 失活、MMP 缺失、Bcl-2-Bax 比例改变以及细胞色素 c 释放发挥抗癌作用。Beta-Sitosterol 调节巨噬细胞极化并减轻小鼠类风湿性炎症。Beta-Sitosterol 在多种癌症小鼠模型中抑制肿瘤生长。Beta-Sitosterol 可用于关节炎、肺癌、乳腺癌等多种癌症、糖尿病等的研究。
    Beta-Sitosterol (purity>98%)
  • HY-N0176
    Dihydroartemisinin

    双氢青蒿素

    Inhibitor 99.03%
    Dihydroartemisinin是一种有效的抗疟疾 (anti-malaria) 活性分子。
    Dihydroartemisinin
  • HY-107910
    Hyaluronidase, Bovine testes

    玻璃酸酶

    Activator
    Hyaluronidase, Bovine testes (Hyaluronate 4-glycanohydrolase; Hyaluronoglucosaminidase) 是一种内糖苷酶 (endoglycosidase),通过裂解糖苷键来解聚 Hyaluronic acid (HA) (HY-B0633A)。Hyaluronidase 降解 HA 并激活膜受体,触发 NF-κB 激活的途径。Hyaluronidase 用于研究与 HA 填充剂注射相关的肉芽肿性异物反应、血管受损所致软组织坏死及简单结节、矫治过度、结节发炎或组织缺血。
    Hyaluronidase, Bovine testes
  • HY-18738
    Pyrrolidinedithiocarbamate ammonium

    吡咯烷二硫代氨基甲酸铵

    Inhibitor ≥98.0%
    Pyrrolidinedithiocarbamate ammonium (Ammonium pyrrolidinedithiocarbamate) 是选择性和具有血脑屏障通透性的 NF-κB 抑制剂。
    Pyrrolidinedithiocarbamate ammonium
  • HY-N1914
    Ergothioneine

    麦角硫因

    Inhibitor 99.98%
    Ergothioneine 是一种具有口服活性的组氨酸甜菜碱的咪唑-2-硫酮衍生物。Ergothioneine 是 p38-MAPKAkt 的特异性抑制剂,在细胞免于应激诱导的凋亡中发挥保护作用。Ergothioneine 具有抗氧化活性。
    Ergothioneine
目录号 产品名 / 同用名 应用 反应物种

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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