目录号 | 产品详情 | 靶点 | |
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T5364 | Apoptosis ERK Others Ferroptosis Nrf2 Autophagy | ||
TBHQ (tert-Butylhydroquinone) 是一种抗氧化剂,可通过对氧化还原敏感的转录因子 Nrf2 诱导抗氧化反应。它也是一种ERK 激活剂,逆转 Dehydrocorydaline 对黑素瘤细胞增殖的抑制作用。 | |||
T2915 | Others Nrf2 | ||
Bardoxolone (CDDO) 是新型核调节因子激活剂。 | |||
T6919 | Apoptosis Others Nrf2 STING | ||
Omaveloxolone (RTA-408) 是一种抗氧化炎症调节剂,可激活Nrf2并抑制一氧化氮。它通过抑制 STING 依赖的 NF-κb 信号通路,来抑制破骨细胞的生成。 | |||
T3227 | Apoptosis Nrf2 Autophagy | ||
Danshensu (Dan shen suan A) 是丹参的有效成分,能够激活 Nrf2信号通路,具有保护心血管作用。 | |||
T0973 | PLK Nrf2 Endogenous Metabolite | ||
Pyridoxine (Vitamin B6) 是一种吡啶衍生物,通过 Nrf-2/HO-1 途径发挥抗氧化作用,作用于阿尔茨海默病细胞模型。 | |||
T80522 | |||
Keap1-Nrf2probe是一款专为检测Keap1-Nrf2相互作用而设计的荧光探针。 | |||
T0492 | Reactive Oxygen Species HIV Protease Nrf2 Endogenous Metabolite Autophagy | ||
Dimethyl fumarate (DMF) 是具有口服活性且可透过血脑屏障的Nrf2激活剂,可诱导抗氧化剂基因表达上调。它是一种富马酸盐衍生物,可作抗炎和免疫调节剂,可研究多发性硬化症。 | |||
TQ0120 | Others Ferroptosis Nrf2 PPAR | ||
CDDO-Im (TP-235) 是一种 Nrf2和 PPAR 的激活剂,对 PPARα 和 PPARγ 的 Ki 分别为232 nM 和 344 nM。 | |||
TN6711 | Others Nrf2 | ||
Toralactone 是一种分离自决明子中的天然产物,通过 Nrf2 依赖性抗氧化机制介导肝脏保护作用。 | |||
T81984 | |||
Keap1-Nrf2-IN-10(compound 15)作为NQO1诱导剂展现出高效性。该化合物能够在γ辐照小鼠中抑制氧化应激,具体机制是通过降低肝脏MDA、ROS及NQO1水平。此外,Keap1-Nrf2-IN-10能显著提升受γ射线照射小鼠的生存率。 |
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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