目录号 | 产品详情 | 靶点 | |
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T61688 | |||
Nrf2 activator-2 (referred to as compound O15), an Osthole derivative, is a highly potent Nrf2 agonist exhibiting an EC 50 of 2.9 μM in 293 T cells. By effectively disrupting the binding between Keap1 and Nrf2, Nrf2 activator-2 activates the Nrf2 pathway. Furthermore, this compound significantly reduces the ubiquitination of Nrf2 in cells, indicating its potential in regulating Nrf2 activity [1]. | |||
T68790 | |||
Shinorine, a mycosporine-like amino acid (MAA), is a small molecule sunscreen produced in some bacteria. Shinorine ameliorates chromium induced toxicity in zebrafish hepatocytes through the facultative activation of Nrf2-Keap1-ARE pathway. Shinorine is also an analogue of porphyra-344. Both porphyra-334 and shinorine are antioxidants and direct antagonists of Keap1-Nrf2 binding. Shinorine may be a useful agent to prevent or retard the progression of multiple degenerative disorders of ageing. Shinorine is a demethyl-analog of Porphyra 334. | |||
T75485 | |||
Dehydrobruceine B 是一种苦木素,可从鸦胆子 (Brucea javanica) 中分离得到。Dehydrobruceine B 与 Cisplatin 通过线粒体途径,协同诱导细胞凋亡 (apoptosis)。Dehydrobruceine B 还增加凋亡诱导因子 (AIF) 和 Bax 表达,抑制 Keap1-Nrf2。 | |||
T64214 | |||
NXPZ-2 是一种口服具有活力的 Keap1-Nrf2protein–protein interaction(PPI) 抑制剂 (Ki: 95 nM, EC50: 120 and 170 nM)。NXPZ-2 能够上调Nrf2含量,并促进其从细胞质向细胞核的易位,表现出对氧化应激的抑制作用。NXPZ-2 能够剂量依赖性地缓解 Aβ[1-42]诱导的认知紊乱,能够提高神经元数量和功能,增强阿尔茨海默病 (AD) 小鼠脑组织的病理改变情况。NXPZ-2 具有潜力进行 Keap1-Nrf2 PPI 抑制剂和 AD 相关的疾病的研究。 | |||
TN3806 | ERK IκB/IKK p38 MAPK TNF NF-κB Akt COX PI3K NADPH DNA/RNA Synthesis Nrf2 JNK Autophagy | ||
Dehydroglyasperin C is a potent NAD(P)H:oxidoquinone reductase (NQO1) and phase 2 enzyme inducer. Dehydroglyasperin C possesses potent antioxidant, cancer chemopreventive, and neuroprotective activities, it has protective effects against chronic diseases |
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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