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

NF-κB

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 Isoform Specific Products:

  • NF-κB

  • NF-κB1/p50

  • RelA/p65

  • RelB

  • c-Rel

Cat. No. Product Name Effect Purity
  • HY-10227
    Bortezomib 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 是第一种用于人体的治疗性蛋白酶体抑制剂,具有抗癌活性。
  • HY-18738
    Pyrrolidinedithiocarbamate ammonium Inhibitor 99.86%
    Pyrrolidinedithiocarbamate ammonium (Ammonium pyrrolidinedithiocarbamate) 是选择性的 NF-κB 抑制剂。
  • HY-P0151
    SN50 Inhibitor
    SN50是可渗透细胞的 NF-κB 易位抑制剂。
  • HY-N0822
    Shikonin 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。
  • HY-32735
    Triptolide Inhibitor 99.79%
    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,抗炎和抗增殖作用。 雷公藤内酯是 NF-κB 活化的抑制剂。
  • HY-126307
    Urolithin B Inhibitor 99.86%
    Urolithin B 是 ellagitannins 的肠道微生物代谢产物之一,具有抗炎和抗氧化作用。Urolithin B 通过降低 IκBα 的磷酸化和降解来抑制NF-κB活性。Urolithin B 抑制 JNKERKAkt 的磷酸化,增强 AMPK 的磷酸化。Urolithin B 也是骨骼肌质量的调节因子。
  • HY-120501
    B022 Inhibitor 98.10%
    B022 是一种有效的选择性的 NF-κB 诱导激酶 (NIK) 抑制剂,Ki 为 4.2 nM。B022 可保护肝脏免受毒素引起的炎症,氧化应激和伤害。
  • HY-N2119
    Sciadopitysin Inhibitor >99.0%
    Sciadopitysin 是一种来自银杏叶片中的双黄酮类化合物。Sciadopitysin 通过抑制 NF-κB 活化并降低 c-FosNFATc1 的表达来抑制 RANKL 诱导的破骨细胞生成和骨丢失。
  • HY-100487
    TAK-243 Inhibitor 99.43%
    TAK-243 (MLN7243) 是一种一流的,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 (ER) 反应,消除 NF-κB 通路活化,促进细胞凋亡。
  • HY-19356
    Rocaglamide Inhibitor 99.34%
    Rocaglamide (Roc-A) 是从 Aglaia 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-13982
    JSH-23 Inhibitor 99.48%
    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-112433
    NIK SMI1 Inhibitor 99.01%
    NIK SMI1 是一种有效的选择性 NF-κB 诱导激酶 (NIK) 抑制剂,可抑制 NIK 催化的 ATP 水解为 ADP,IC50 为 0.23±0.17 nM。
  • HY-N0176
    Dihydroartemisinin Inhibitor 99.03%
    Dihydroartemisinin是一种有效的抗疟疾 (anti-malaria) 药物。
  • HY-10257
    BAY 11-7085 Inhibitor 99.99%
    BAY 11-7085是NF-κB激活和IκBα磷酸化的抑制剂,稳定IκBα的IC50值为10 μM。
  • HY-14655
    Sulfasalazine Inhibitor 99.42%
    Sulfasalazine是治疗类风湿关节炎和溃疡性结肠炎的药物。报道显示Sulfasalazine可抑制 NF-κB 的活性。
  • HY-N2149
    Tomatidine Inhibitor >98.0%
    Tomatidine 通过阻断 NF-κBJNK 信号发挥抗炎作用。
  • HY-N0141
    Parthenolide Inhibitor 99.88%
    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-14645
    (-)-DHMEQ Inhibitor 98.72%
    (–)-DHMEQ 是一种有效的 NF-κB 抑制剂。
  • HY-N0197
    Baicalin Inhibitor 98.92%
    Baicalin 是一种从 Scutellaria baicalensis 中分离出来的类黄酮糖苷。Baicalin 降低 NF-κB 表达。
  • HY-N0274
    Caffeic acid phenethyl ester Inhibitor 99.67%
    Caffeic acid phenethyl ester 是一种 NF-κB 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.

Isoform Specific Products

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