2. Signaling Pathways
  3. NF-κB
  4. 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.

NF-κB 亚型特异性产品:

NF-κB Isoform Comparison
Cat. No. Product Name Effect Purity Chemical Structure
  • HY-15122AR
    Sinomenine hydrochloride (Standard)

    盐酸青藤碱 (Standard)

    		Inhibitor
    Sinomenine hydrochloride (Standard) 是 Sinomenine hydrochloride 的分析标准品。本产品用于研究及分析应用。Sinomenine hydrochloride (Cucoline hydrochloride) 是来自 Sinomenium acutum 的一种生物碱，是 NF-κB 活化的阻断剂。Sinomenine 也是 μ 阿片受体 (μ-opioid receptor) 激活剂。
    Sinomenine hydrochloride (Standard)
  • HY-N0392R
    Polygalasaponin F (Standard)

    瓜子金皂苷己 (Standard)

    		Inhibitor
    Polygalasaponin F (Standard) 是 Polygalasaponin F 的分析标准品。本产品用于研究及分析应用。Polygalasaponin F 是一种从 Polygala japonica 提取的齐墩果烷型三萜皂苷，可降低炎性细胞因子肿瘤坏死因子 α (TNFa) 的释放。 Polygalasaponin F 通过调节 TLR4-PI3K/AKT-NF-kB 信号通路减少神经炎症细胞因子的分泌。
    Polygalasaponin F (Standard)
  • HY-N8719
    Pratol

    7-羟基-4'-甲氧基黄酮

    		Inhibitor
    Pratol 是有效的 NF-κB 抑制剂。Pratol 显著降低了 LPS 刺激的 RAW 264.7 细胞中 NO 和前列腺素 PGE2 的产生，且无细胞毒性。Pratol 能减少促炎细胞因子。Pratol 可用于炎性疾病和癌症的研究。
    Pratol
  • HY-162805
    iNOS/TopoI-IN-1 Inhibitor
    iNOS/TopoI-IN-1 (compound AuL9) 是一种多靶点杂交分子，具有抗肿瘤，抗炎和抗氧化活性。iNOS/TopoI-IN-1 在体外抑制乳腺癌细胞 MCF-7 和 MDA MB-231 的生长，IC50 值分别为 3.5 μM 和 6.3 μM，并通过抑制人类拓扑异构酶I (TopoI) (Ki=2.72 μM) 引发 DNA 损伤并诱导乳腺癌细胞凋亡 (apoptosis)。此外，NOS/TopoI-IN-1 通过抑制了 NF-kB 的活化，来抑制 iNOS 的表达 (Ki=1.49 μM)。
    iNOS/TopoI-IN-1
  • HY-107352S
    Fosfenopril-d7

    福辛普利拉EP杂质A)-d7

    Fosfenopril-d7 是 Fosfenopril 氘代物。
    Fosfenopril-d<sub>7</sub>
  • HY-N2098R
    Obtusifolin (Standard)

    决明蒽醌 (Standard)

    		Inhibitor
    Obtusifolin (Standard) 是 Obtusifolin 的分析标准品。本产品用于研究及分析应用。Obtusifolin 是从决明子的种子中分离出，通过抑制 NF-kB 通路来调节气道上皮细胞中 MUC5AC 粘蛋白的基因表达和产生。Obtusifolin 通过靶向甲状旁腺激素相关蛋白来抑制邻苯二甲酸酯诱导的乳腺癌骨转移。
    Obtusifolin (Standard)
  • HY-N9149
    Cryptanoside A Inducer
    Cryptanoside A 是一种强心苷环氧化物，可以从 Cryptolepis dubia 的茎中分离出来。Cryptanoside A 对癌细胞具有有效的细胞毒性。Cryptanoside A 还抑制 Na+/K+-ATPase 活性。Cryptanoside A 增加 Akt, NF-κB p65 亚基的表达。
    Cryptanoside A
  • HY-N6607R
    Tryptanthrin (Standard) Inhibitor
    Tryptanthrin (Standard) 是 Tryptanthrin 的分析标准品。本产品用于研究及分析应用。Tryptanthrin 是一种吲哚喹唑啉，可以是产自靛蓝植物的生物碱。Tryptanthrin 是一种口服有效的细胞白三烯 (LT) 生物合成抑制剂。Tryptanthrin 具有抗癌活性。Tryptanthrin 可抑制 NOS1、COX-2、NF-κB 的表达水平，调节 IL-2、IL-10、TNF-α 的表达水平。
    Tryptanthrin (Standard)
  • HY-N11775
    Eudebeiolide B Inhibitor
    Eudebeiolide B 是一种可以从荔枝草中分离出来的化合物。Eudebeiolide B 通过调节 RANKL 诱导的 NF-κB、c-Fos 和钙信号，抑制破骨细胞生成，可用于破骨细胞相关疾病的研究。
    Eudebeiolide B
  • HY-149351
    NF-κB-IN-10 Inhibitor
    NF-κB-IN-10 (化合物 E1) 是一种 NF-κB 抑制剂，可通过调节 Nrf2/NF-κB 信号通路减少氧化应激和炎症，从而改善心力衰竭。NF-κB-IN-10 可抑制 RAW264.7 细胞中 LPS 诱导的 NO 产生以及 iNOS 和 COX-2 的表达。NF-κB-IN-10 可用于心血管疾病的研究。
    NF-κB-IN-10
  • HY-155759
    HMGB1-IN-2 Inhibitor
    HMGB1-IN-2 (compound 15) 是高度保守的核蛋白 HMGB1 的抑制剂，在 RAW264.7 细胞中显示出 NO 抑制作用，IC50 值为 20.2 μM。 HMGB1-IN-2 (30 μM) 降低 IL-1 β、TNF-α、caspase-1 p20 的水平，抑制 NF-κB p65 的磷酸化，具有抗凋亡活性。 HMGB1-IN-2（15 mg/kg；腹腔注射）可缓解脓毒症急性肾损伤小鼠的肾损伤。HMGB1-IN-2 抑制 Huh7 细胞和 A549 细胞的 IC50 分别为 77.0 μM 和 82.0 μM。
    HMGB1-IN-2
  • HY-149838
    NF-κB-IN-9 Inhibitor
    NF-κB-IN-9 是一种靶向核因子 NF-κB 的声敏剂 (λex/λem=489/628 nm)。NF-κB-IN-9 由于分子中有两个白藜芦醇单元，而对 NF-κB 信号表现出强烈的抑制作用。NF-κB-IN-9 具有抗肿瘤活性，并对癌细胞表现出显着的声细胞毒性。NF-κB-IN-9 在小鼠移植模型中具有生物安全性。
    NF-κB-IN-9
  • HY-N0603R
    20(S)-Ginsenoside Rg3 (Standard)

    20(S)-人参皂苷 Rg3 (Standard)

    		Inhibitor
    20(S)-Ginsenoside Rg3 (Standard)是 20(S)-Ginsenoside Rg3 的分析标准品。本产品用于研究及分析应用。20(S)-Ginsenoside Rg3 是人参的主要成分。20(S)-Ginsenoside Rg3 抑制 Na+ 和 hKv1.4 通道，IC50 分别为 32.2±4.5 和 32.6±2.2 μM。20(S)-Ginsenoside Rg3 还抑制 Aβ<
    20(S)-Ginsenoside Rg3 (Standard)
  • HY-N1380S4
    Guaiacol-d4-1

    愈创木酚-d4-1

    Guaiacol-d4-1 是 Guaiacol 的氘代物。 Guaiacol 是一种酚类化合物，抑制 LPS 刺激的 COX-2 表达和 NF-κB 激活。具有抗炎活性。
    Guaiacol-d<sub>4</sub>-1
  • HY-N0807R
    Swertiamarin (Standard)

    獐牙菜苦苷 (Standard)

    		Modulator
    Swertiamarin (Standard) 是 Swertiamarin 的分析标准品。本产品用于研究及分析应用。Swertiamarin 是一种口服有效的环烯醚萜化合物，具有降血糖、降血脂、抗风湿、抗氧化活性，可用于糖尿病、关节炎疾病的研究。
    Swertiamarin (Standard)
  • HY-153762
    COX-2-IN-32 Inhibitor
    COX-2-IN-32 (Compound 2f) 是一种 iNOS 和 COX-2 抑制剂。COX-2-IN-32 降低 NF-κB 的表达。COX-2-IN-32 可抑制 LPS 诱导的 RAW264.7 巨噬细胞中 NO 的产生 (IC50: 11.2 μM)，具有抗炎活性。
    COX-2-IN-32
  • HY-142100
    Licoagrochalcone C Inhibitor
    Licoagrochalcone C 是一种类黄酮，对 NF-κB 转录有抑制活性。Licoagrochalcone C 对 LPS (HY-D1056) 诱导的 NO 产生具有显着的抑制活性。
    Licoagrochalcone C
  • HY-N3552
    Catalposide Inhibitor ≥98.0%
    Catalposide 是可从 Catalpa ovate G. Don 分离得到的环烯醚萜苷，可抑制 LPS 诱导的TNF-α、IL-1β、IL-6 和 NF-κB (p65) 的活化。
    Catalposide
  • HY-146560
    Xanthine oxidase-IN-6 Inhibitor
    Xanthine oxidase-IN-6 (Compound 6c) 是一种强效的、具有口服活性的黄嘌呤氧化酶 (XOD) 混合型抑制剂，其 IC50 值为1.37 µM。Xanthine oxidase-IN-6 具有很强的抗高尿酸血症 (anti-hyperuricemia) 和肾保护活性。
    Xanthine oxidase-IN-6
  • HY-149472
    Anti-osteoporosis agent-4 Inhibitor
    Anti-osteoporosis agent-4 (Compound 11h) 抑制原代破骨细胞的分化。Anti-osteoporosis agent-4 (Compound 11h) 减弱 RANKL 诱导的破骨细胞生成。Anti-osteoporosis agent-4 抑制破骨细胞形成，IC50值为 358.29 nM。Anti-osteoporosis agent-4 抑制 PI3K/AKT 和 IκBα/NF-κB 信号通路激活。
    Anti-osteoporosis agent-4
目录号 产品名 / 同用名 应用 反应物种
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Download NF-κB Signaling Pathway Map.

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.

NF-κB Isoform Comparison

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