目录号 | 产品详情 | 靶点 | |
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T3849 | Apoptosis Nrf2 | ||
Kinsenoside ((+)-Kinsenoside) 是从金盏花属植物中分离得到的主要活性成分,以 Nrf2 依赖的方式保护髓核细胞在氧化应激下的生存能力,防止细胞凋亡、衰老和线粒体功能障碍。它显示出显着的抗肝毒性和抗炎活性。 | |||
T16331 | Others Nrf2 | ||
NK-252 是潜在的 Nrf2激活剂,具有很好的Nrf2活化活性。 | |||
T6S0232 | Influenza Virus DNA/RNA Synthesis Nrf2 Endogenous Metabolite | ||
Eriodictyol (Huazhongilexone) 是从中草药中得到的一种黄酮类天然产物,具有抗氧化、抗炎和抗糖尿病作用。它还是一种流感依赖 RNA 的RNA 聚合酶抑制剂,IC50为 18 nM。它可诱导Nrf2信号通路。 | |||
T6S2356 | Nrf2 AChE | ||
Corynoline ((+)-Corynoline) 是可逆和非竞争性的乙酰胆碱酯酶抑制剂,IC50=30.6 μM。它可激活 Nrf2,具有抗炎作用。 | |||
TQ0211 | Others Ferroptosis Nrf2 | ||
Brusatol (NSC-172924) 是一种从鸦胆子植物中分离出来的天然产物,抑制Nrf2通路,可使多种癌细胞对 Cisplatin 和其他化疗药物敏感。它可开发为辅助化疗化合物,可增加细胞凋亡。 | |||
T3012 | Apoptosis Others NF-κB Nrf2 | ||
Mangiferin (Hedysarid) 是一种Nrf2激活剂。它抑制NF-κB 亚基p65和p50的核移位,具有抗氧化、抗糖尿病、抗高尿酸血症、抗病毒、抗癌和抗炎活性。 | |||
T1027 | Apoptosis Nrf2 Endogenous Metabolite PDE Autophagy | ||
Luteolin (Luteolol) 属于黄酮类天然产物,是一种 Nrf2 抑制剂、PDE 抑制剂。Luteolin 具有多种生物活性,包括抗肿瘤、抗氧化、抗炎、抗菌、抗病毒、抗过敏和促凝血等。 | |||
TN6339 | Others | ||
(R)-5-Hydroxy-1,7-diphenylheptan-3-one ((5R)-Dihydroyashabushiketol) 是从中药材高良姜的根茎中提取的。它抑制茶碱刺激的鼠 B16 黑色素瘤 4A5 细胞中的黑色素生成。 | |||
T1593 | Others Nrf2 NPC1L1 Autophagy | ||
Ezetimibe (SCH 58235) 是一种膳食胆固醇吸收抑制剂。它是一种NPC1L1抑制剂,是有效的Nrf2激活剂。 | |||
T2915 | Others Nrf2 | ||
Bardoxolone (CDDO) 是新型核调节因子激活剂。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-02101 | KEAP1 Protein, Human, Recombinant (His & GST & Avi) | Human | Baculovirus-Insect Cells | ||
Kelch-like ECH-associated protein 1, also known as a cytosolic inhibitor of Nrf2, Kelch-like protein 19, KEAP1, and INRF2, is a cytoplasm and nucleus protein that contains one BACK (BTB/Kelch associated) domain, one BTB (POZ) domain, and six Kelch repeats. KEAP1 / INRF2 is broadly expressed, with the highest levels in skeletal muscle. KEAP1 / INRF2 is a key regulator of the NRF2 transcription factor, which transactivates the antioxidant response element (ARE) and upregulates numerous proteins involved in antioxidant defense. Under basal conditions, KEAP1 / INRF2 targets NRF2 for ubiquitination and proteolytic degradation and as such is responsible for the rapid turnover of NRF2. KEAP1 / INRF2 retains NFE2L2 / NRF2 in the cytosol. KEAP1 / INRF2 functions as a substrate adapter protein for the E3 ubiquitin ligase complex formed by CUL3 and RBX1. It targets NFE2L2 / NRF2 for ubiquitination and degradation by the proteasome, thus resulting in the suppression of its transcriptional activity and the repression of antioxidant response element-mediated detoxifying enzyme gene expression. KEAP1 / INRF2 may also retain BPTF in the cytosol. It targets PGAM5 for ubiquitination and degradation by the proteasome.
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TMPY-03888 | KEAP1 Protein, Human, Recombinant (His & GST) | Human | Baculovirus-Insect Cells | ||
Kelch-like ECH-associated protein 1, also known as a cytosolic inhibitor of Nrf2, Kelch-like protein 19, KEAP1, and INRF2, is a cytoplasm and nucleus protein that contains one BACK (BTB/Kelch associated) domain, one BTB (POZ) domain, and six Kelch repeats. KEAP1 / INRF2 is broadly expressed, with the highest levels in skeletal muscle. KEAP1 / INRF2 is a key regulator of the NRF2 transcription factor, which transactivates the antioxidant response element (ARE) and upregulates numerous proteins involved in antioxidant defense. Under basal conditions, KEAP1 / INRF2 targets NRF2 for ubiquitination and proteolytic degradation and as such is responsible for the rapid turnover of NRF2. KEAP1 / INRF2 retains NFE2L2 / NRF2 in the cytosol. KEAP1 / INRF2 functions as a substrate adapter protein for the E3 ubiquitin ligase complex formed by CUL3 and RBX1. It targets NFE2L2 / NRF2 for ubiquitination and degradation by the proteasome, thus resulting in the suppression of its transcriptional activity and the repression of antioxidant response element-mediated detoxifying enzyme gene expression. KEAP1 / INRF2 may also retain BPTF in the cytosol. It targets PGAM5 for ubiquitination and degradation by the proteasome.
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TMPY-03432 | KEAP1 Protein, Human, Recombinant | Human | Baculovirus-Insect Cells | ||
Kelch-like ECH-associated protein 1, also known as a cytosolic inhibitor of Nrf2, Kelch-like protein 19, KEAP1, and INRF2, is a cytoplasm and nucleus protein that contains one BACK (BTB/Kelch associated) domain, one BTB (POZ) domain, and six Kelch repeats. KEAP1 / INRF2 is broadly expressed, with the highest levels in skeletal muscle. KEAP1 / INRF2 is a key regulator of the NRF2 transcription factor, which transactivates the antioxidant response element (ARE) and upregulates numerous proteins involved in antioxidant defense. Under basal conditions, KEAP1 / INRF2 targets NRF2 for ubiquitination and proteolytic degradation and as such is responsible for the rapid turnover of NRF2. KEAP1 / INRF2 retains NFE2L2 / NRF2 in the cytosol. KEAP1 / INRF2 functions as a substrate adapter protein for the E3 ubiquitin ligase complex formed by CUL3 and RBX1. It targets NFE2L2 / NRF2 for ubiquitination and degradation by the proteasome, thus resulting in the suppression of its transcriptional activity and the repression of antioxidant response element-mediated detoxifying enzyme gene expression. KEAP1 / INRF2 may also retain BPTF in the cytosol. It targets PGAM5 for ubiquitination and degradation by the proteasome.
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TMPH-01788 | NFE2L2 Protein, Human, Recombinant (His) | Human | E. coli | ||
Transcription factor that plays a key role in the response to oxidative stress: binds to antioxidant response (ARE) elements present in the promoter region of many cytoprotective genes, such as phase 2 detoxifying enzymes, and promotes their expression, thereby neutralizing reactive electrophiles. In normal conditions, ubiquitinated and degraded in the cytoplasm by the BCR(KEAP1) complex. In response to oxidative stress, electrophile metabolites inhibit activity of the BCR(KEAP1) complex, promoting nuclear accumulation of NFE2L2/NRF2, heterodimerization with one of the small Maf proteins and binding to ARE elements of cytoprotective target genes. The NFE2L2/NRF2 pathway is also activated in response to selective autophagy: autophagy promotes interaction between KEAP1 and SQSTM1/p62 and subsequent inactivation of the BCR(KEAP1) complex, leading to NFE2L2/NRF2 nuclear accumulation and expression of cytoprotective genes. May also be involved in the transcriptional activation of genes of the beta-globin cluster by mediating enhancer activity of hypersensitive site 2 of the beta-globin locus control region. Plays also an important role in the regulation of the innate immune response and antiviral cytosolic DNA sensing. It is a critical regulator of the innate immune response and survival during sepsis by maintaining redox homeostasis and restraint of the dysregulation of proinflammatory signaling pathways like MyD88-dependent and -independent and TNF-alpha signaling. Suppresses macrophage inflammatory response by blocking proinflammatory cytokine transcription and the induction of IL6. Binds to the proximity of proinflammatory genes in macrophages and inhibits RNA Pol II recruitment. The inhibition is independent of the NRF2-binding motif and reactive oxygen species level. Represses antiviral cytosolic DNA sensing by suppressing the expression of the adapter protein STING1 and decreasing responsiveness to STING1 agonists while increasing susceptibility to infection with DNA viruses. Once activated, limits the release of pro-inflammatory cytokines in response to human coronavirus SARS-CoV-2 infection and to virus-derived ligands through a mechanism that involves inhibition of IRF3 dimerization. Also inhibits both SARS-CoV-2 replication, as well as the replication of several other pathogenic viruses including Herpes Simplex Virus-1 and-2, Vaccinia virus, and Zika virus through a type I interferon (IFN)-independent mechanism.
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