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NF-κB

Nuclear factor-κB; Nuclear factor-kappaB

NF-κB

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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 Isoform Comparison
Art. -Nr. Produktname Wirkung Reinheit Chemical Structure
  • HY-171239
    Ste2Cys
    		Activator
    Ste2Cys is a diacylglycerol cysteine-type immunologic adjuvant lipid molecule. Ste2Cys can bind to TLR2 and activate NF-κB signaling pathway. Ste2Cy can upregulate the expression of MHC II class molecules on the surface of mouse bone marrow-derived D1 dendritic cells. Ste2Cys can be used for research of the development of immunologic vaccines.
    Ste2Cys
  • HY-182064
    EGFR-IN-206
    		Inhibitor
    EGFR-IN-206 is an orally active EGFR inhibitor. EGFR-IN-206 inhibits the phosphorylation of the key tumor growth protein EGFR, and suppresses the proliferation, migration and invasion of EGFR triple-mutant tumor cell lines. EGFR-IN-206 downregulates the expression of inflammation-related proteins iNOS, COX-2 and NF-κB (p65). EGFR-IN-206 promotes the secretion of NO. EGFR-IN-206 reduces the secretion of IL-6. EGFR-IN-206 induces apoptosis (apoptosis) of EGFR triple-mutant tumor cells. EGFR-IN-206 exerts antitumor activity in EGFR triple-mutant mice. EGFR-IN-206 is applicable to the research of non-small cell lung cancer.
    EGFR-IN-206
  • HY-180952
    Zaltoprofen sulfoxide
    		Inhibitor
    Zaltoprofen sulfoxide (Compound M2) is the main metabolite of Zaltoprofen (HY-B0619). Zaltoprofen sulfoxide is an efficient and selective COX-2 inhibitor (IC50 = 45.38 nM) and a PPAR-γ activator. Zaltoprofen sulfoxide effectively inhibits NF-κB and MAPK inflammatory signaling pathways and alleviates acute lung injury induced by LPS (HY-D1056B3). Zaltoprofen sulfoxide can be used for the study of acute lung injury.
    Zaltoprofen sulfoxide
  • HY-P10850
    PIYLGGVFQ
    		Inhibitor
    PIYLGGVFQ is a peptide inhibitor for TNF-α. PIYLGGVFQ inhibits TNF-α-mediated apoptosis, NF-κB nuclear translocation and activation. PIYLGGVFQ exhibits anti-arthritic activity in the CIA mouse model.
    PIYLGGVFQ
  • HY-163778
    ZM600
    		Inhibitor
    ZM600 is a potent and orally active antihepatic fibrosis agent. ZM600 decreases the LPS (HY-D1056) induced protein expression of collagen I, α-SM, p-p65. ZM600 has the potential for the research of liver fibrosis.
    ZM600
  • HY-Y1362R
    Ethyl pyruvate (Standard)
    		Inhibitor
    Ethyl pyruvate (Standard) is the analytical standard of Ethyl pyruvate. This product is intended for research and analytical applications. Ethyl pyruvate is a simple derivative of the endogenous metabolite pyruvate. Ethyl pyruvate is an HMGB1 release inhibitor. Ethyl pyruvate can induce apoptosis by autophagy. Ethyl pyruvate has anti-inflammatory, antioxidant and anti-tumor activity. Ethyl pyruvate can be used in the study of neurodegenerative diseases such as Alzheimer's and Parkinson's disease.
    Ethyl pyruvate (Standard)
  • HY-101200R
    Linsidomine hydrochloride (Standard)
    		Activator
    Linsidomine (hydrochloride) (Standard) is the analytical standard of Linsidomine (hydrochloride). This product is intended for research and analytical applications. Linsidomine hydrochloride (SIN-1 chloride) is a spontaneous ROS/RNS generator and peroxynitrite donor. Linsidomine hydrochloride is a vasodilator and platelet aggregation inhibitor. Linsidomine hydrochloride induces oxidative stress-induced chondrocyte apoptosis and necrosis. Linsidomine hydrochloride inhibits the migration, proliferation and neointima formation of vascular smooth muscle cells by inhibiting the expression of annexin A2. In addition, low doses of Linsidomine hydrochloride shows protective effects on Zn2+ treated nerve cells.
    Linsidomine hydrochloride (Standard)
  • HY-182283
    sEH-IN-23
    		Inhibitor
    sEH-IN-23 is a soluble epoxide hydrolase inhibitor with a IC50 of 0.8 nM against human sEH and 0.7 nM against murine sEH. sEH-IN-23 inhibits inflammatory factor production mediated by NF-κB activation, reactive oxygen species (ROS) generation, and the release of pro-inflammatory cytokines IL-1β, IL-6 and TNF-α. sEH-IN-23 exhibits anti-inflammatory activity in acute lung injury models. sEH-IN-23 can be used for the research of acute lung injury.
    sEH-IN-23
  • HY-174257
    RCD405
    		Inhibitor
    RCD405 is a bronchodilator. RCD405 exerts relaxant effects by acting directly on human airway smooth muscle (hASM) with an EC50 value of 12 μM for histamine-induced contractions and 45.71 μM for carbachol-induced contractions. RCD405 inhibits cholinergic and histaminergic tone and reduces electrically stimulated (EFS)-induced contractions. RCD405 is promising for research of asthma and chronic obstructive pulmonary disease (COPD).
    RCD405
  • HY-122007
    AM-0561
    		Inhibitor
    AM-0561 is a NIK inhibitor (Ki: 0.3 nM). AM-0561 decreases p52 levels.
    AM-0561
  • HY-N8290R
    Lactupicrin (Standard)
    		Inhibitor
    Lactupicrin (Standard) is the analytical standard of Lactupicrin. This product is intended for research and analytical applications. Lactupicrin (Lactucopicrin) exhibits analgesic, sedative, antimalarial activities and atheroprotective effect. Lactupicrin inhibits acetylcholinesterase (AChE) with an IC50 of 150.3 μM. Lactupicrin is an orally active characteristic bitter sesquiterpene lactone.
    Lactupicrin (Standard)
  • HY-P1832
    PTD-p65-P1 Peptide
    		Inhibitor
    PTD-p65-P1 Peptide is a potent, selective nuclear transcription factor NF-κB inhibitor and derives from the p65 subunit of NF-κB amino acid residues 271-282, which selectively inhibits NF-κB activation induced by various inflammatory stimulation, down-regulate NF-κB-mediated gene expression and up-regulate apoptosis.
    PTD-p65-P1 Peptide
  • HY-128853R
    Taurodeoxycholate sodium salt (Standard)
    		Inhibitor
    Taurodeoxycholate sodium salt (Standard) is a bile salt (Standard)-related anionic detergent. Taurodeoxycholate sodium salt (Standard) is formed in the liver by conjugation of deoxycholate with Taurine (HY-B0351). Taurodeoxycholate sodium salt (Standard) is used for isolation of membrane proteins including inner mitochondrial membrane proteins. Taurodeoxycholate (TDCA) exhibits anti-inflammatory and neuroprotective effects.
    Taurodeoxycholate sodium salt (Standard)
  • HY-N0220R
    Dauricine (Standard)
    		Inhibitor
    Dauricine (Standard) is the analytical standard of Dauricine. This product is intended for research and analytical applications. Dauricine, a bisbenzylisoquinoline alkaloid in Menispermum dauricum, possesses anti-inflammatory activity. Dauricine inhibits cell proliferation and invasion, and induces apoptosis by suppressing NF-κB activation in a dose-and time-dependent manner in colon cancer.
    Dauricine (Standard)
  • HY-162963
    DN203316
    		Inhibitor
    DN203316 (PPARδ agonist 11) is a potent, selective, orally active PPARδ agonist (EC50 = 20 nM) with high selectivity over PPARα and PPARγ. DN203316 suppresses NF-κB-mediated inflammatory signaling, inhibits ferroptosis by upregulating xCT and GPX4, and attenuates STING-TBK1-IRF3-driven fibrogenic responses. DN203316 is useful for research on inflammatory disorders, metabolic dysfunction-associated steatohepatitis (MASH), and liver fibrosis.
    DN203316
  • HY-N17353
    Vitedoamine A
    		Inhibitor
    Vitedoamine A is a Phenylnaphthalene-type lignan alkaloid. Vitedoamine A can be isolated from Vitex negundo. Vitedoamine A inhibits the activity of IKKβ with an IC50 value of 39 μM. Vitedoamine A could inhibit the transcriptional activity of NF-κB, and suppress the production of NO and reduce the expressions of inflammatory cytokines (IL-1β, IL-6, and TNF-α). Vitedoamine A inhibits the phosphorylation of IKKα/β and p65, and prevents the degradation of IκBα. Vitedoamine A possesses anti-rheumatoid arthritis capacity.
    Vitedoamine A
  • HY-163775
    Anti-inflammatory agent 88
    		Agonist
    Anti-inflammatory agent 88 (compound 6) is a carbazole derivative with anti-inflammatory activity found in marine Streptomyces. It exerts its anti-inflammatory effect by inhibiting pro-inflammatory factors and enhancing the expression of anti-inflammatory factors in the Myd88/Nf-κB pathway. Anti-inflammatory agent 88 can be used for the development of anti-inflammatory drugs.
    Anti-inflammatory agent 88
  • HY-115797
    LQFM030
    		Inhibitor
    LQFM030 is a novel small molecule MDM2 inhibitor. LQFM030 exhibits concentration dependent cytotoxicity in K562 cells (IC50 = 0.28 mM). LQFM030 induces cell apoptosis through G0/G1 phase cell cycle arrest and increased Caspase activity. LQFM030 downregulates the mRNA expression of MDM2, MDMX, p73, MYC, and NF-κB. LQFM030 is commonly used in research on cancers such as leukemia.
    LQFM030
  • HY-N3497
    Isochamaejasmin
    		Activator
    Isochamaejasmin is a biflavonoid with anti-cancer, antiplasmodial and insecticidal activities. Isochamaejasmin displays a potent NF-κB (NF-κB) activation activity. Isochamaejasmin could cause DNA damage and induce apoptosis via the mitochondrial pathway in AW1 cells. Isochamaejasmin also has a moderate antiplasmodial activity (IC50 of 7.3 μM for P. falciparum) and relatively low cytotoxicity (CC50 of 29.0 μM).
    Isochamaejasmin
  • HY-P5641
    Pleurocidin
    		Inhibitor 98.91%
    Pleurocidin is an Antimicrobial peptide. Pleurocidin is derived from the skin mucosa or intestinal secretions of Pseudopleuronectes americanus. Pleurocidin inhibits the expression of key proteins in the MAPK and NF-κB inflammatory signaling pathways. Pleurocidin alters serum inflammatory and immune cytokine levels, regulates the down-regulation of tight junction proteins, and modulates the intestinal flora. Pleurocidin exerts antibacterial activity by inducing bacterial membrane damage, hydroxyl radical formation, and NADH depletion, and also produces a synergistic effect with Antibiotics. Pleurocidin alleviates DSS-induced ulcerative colitis. Pleurocidin can be used for research on ulcerative colitis, bacterial infections, and bacterial biofilm-related infections.
    Pleurocidin
Art. -Nr. Produktname / Synonyms Application Reactivity
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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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