KEAP1 Protein, Human (sf9)
目录号 : GP27282BCR E3 泛素连接酶复合物中的 KEAP1 通过泛素化 NFE2L2/NRF2 来调节细胞对氧化应激的反应。作为氧化应激传感器，KEAP1 通常会促进 NFE2L2/NRF2 降解。KEAP1 蛋白, Human (sf9) 是重组的 KEAP1 蛋白，由 Sf9 insect cells 表达，不带标签。
Sample solution is provided at 25 µL, 10mM.
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KEAP1 in the BCR E3 ubiquitin ligase complex complex regulates cellular responses to oxidative stress by ubiquitinating NFE2L2/NRF2. As an oxidative stress sensor, KEAP1 normally promotes NFE2L2/NRF2 degradation. KEAP1 Protein, Human (sf9) is the recombinant human-derived KEAP1 protein, expressed by Sf9 insect cells , with tag free.
KEAP1, as the substrate-specific adapter within the BCR (BTB-CUL3-RBX1) E3 ubiquitin ligase complex, intricately regulates the cellular response to oxidative stress by orchestrating the ubiquitination of NFE2L2/NRF2. Serving as a crucial sensor for oxidative and electrophilic stress, KEAP1, under normal conditions, facilitates the ubiquitination and subsequent degradation of NFE2L2/NRF2, a transcription factor essential for the expression of numerous cytoprotective genes. When confronted with oxidative stress, distinct electrophile metabolites induce non-enzymatic covalent modifications on highly reactive cysteine residues in KEAP1, effectively dampening the ubiquitin ligase activity of the BCR(KEAP1) complex. This disruption promotes the nuclear accumulation of NFE2L2/NRF2 and triggers the expression of phase II detoxifying enzymes. Furthermore, selective autophagy leads to the sequestration of KEAP1 in inclusion bodies through its interaction with SQSTM1/p62, resulting in the inactivation of the BCR(KEAP1) complex and the activation of NFE2L2/NRF2. Notably, the BCR(KEAP1) complex extends its ubiquitin ligase activity to substrates like SQSTM1/p62, BPTF, and PGAM5, modulating their degradation via the proteasome. The ubiquitin ligase activity of the BCR(KEAP1) complex faces inhibition in response to oxidative stress and electrophile metabolites such as sulforaphane, as these metabolites react with reactive cysteine residues in KEAP1, leading to the non-enzymatic covalent modifications that incapacitate the complex. Moreover, selective autophagy contributes to the inactivation of the BCR(KEAP1) complex through the interaction between KEAP1 and SQSTM1/p62, promoting the sequestration of the complex in inclusion bodies and facilitating its degradation.
| Purity | Greater than 85% as determined by reducing SDS-PAGE | Source | Sf9 insect cells |
| Phycical Appearance | Lyophilized powder | Shipping Condition | Room temperature in continental US; may vary elsewhere. |
| Synonyms | KEAP1 蛋白;Kelch-like ECH-associated protein 1; Cytosolic inhibitor of Nrf2; KEAP1; KEAP1 | ||
| Amino Acid Sequence | QPDPRPSGAGACCRFLPLQSQCPEGAGDAVMYASTECKAEVTPSQHGNRTFSYTLEDHTKQAFGIMNELRLSQQLCDVTLQVKYQDAPAAQFMAHKVVLASSSPVFKAMFTNGLREQGMEVVSIEGIHPKVMERLIEFAYTASISMGEKCVLHVMNGAVMYQIDSVVRACSDFLVQQLDPSNAIGIANFAEQIGCVELHQRAREYIYMHFGEVAKQEEFFNLSHCQLVTLISRDDLNVRCESEVFHACINWVKYDCEQRRFYVQALLRAVRCHSLTPNFLQMQLQKCEILQSDSRCKDYLVKIFEELTLHKPTQVMPCRAPKVGRLIYTAGGYFRQSLSYLEAYNPSDGTWLRLADLQVPRSGLAGCVVGGLLYAVGGRNNSPDGNTDSSALDCYNPMTNQWSPCAPMSVPRNRIGVGVIDGHIYAVGGSHGCIHHNSVERYEPERDEWHLVAPMLTRRIGVGVAVLNRLLYAVGGFDGTNRLNSAECYYPERNEWRMITAMNTIRSGAGVCVLHNCIYAAGGYDGQDQLNSVERYDVETETWTFVAPMKHRRSALGITVHQGRIYVLGGYDGHTFLDSVECYDPDTDTWSEVTRMTSGRSGVGVAVTMEPCRKQIDQQNCTC | ||
| Apparent Molecular Weight | Approximately 64-67 kDa | ||
| Stability | Stored at -20°C for 2 years from date of receipt. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage. | ||
| Biological Activity | Measured by its ability to inhibit the proliferation of A549 cells. The ED50 for this effect is 1.117-2.321 μg/mL. | ||
| Endotoxin Level | <1 EU/μg, determined by LAL method. | ||
| Reconstitution | It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH2O. For long term storage it is recommended to add a carrier protein (0.1% BSA, 5% HSA, 10% FBS or 5% Trehalose). | ||
| Formulation | Lyophilized from a 0.22 μm filtered solution of 20 mM Tris, 500 mM NaCl, 3 mM DTT, 10% Glycerol, pH 7.4 or 50 mM Tris-HCl, 500 mM NaCl, pH 8.0, 20% Glycerol. Note: For SPR assay, please replace the buffer. Primary amine components (e.g., Tris, imidazole) | ||
KEAP1 作为 BCR (BTB-CUL3-RBX1) E3 泛素连接酶复合物内的底物特异性接头，通过协调 NFE2L2/NRF2 的泛素化来复杂地调节细胞对氧化应激的反应。作为氧化和亲电应激的重要传感器，KEAP1 在正常条件下促进 NFE2L2/NRF2 的泛素化和随后的降解，NFE2L2/NRF2 是许多细胞保护基因表达所必需的转录因子。当面临氧化应激时，不同的亲电子代谢物会诱导 KEAP1 中高反应性半胱氨酸残基发生非酶促共价修饰，从而有效抑制 BCR(KEAP1) 复合物的泛素连接酶活性。这种破坏促进 NFE2L2/NRF2 的核积累并触发 II 相解毒酶的表达。此外，选择性自噬通过与 SQSTM1/p62 的相互作用导致 KEAP1 被隔离在包涵体中，从而导致 BCR(KEAP1) 复合物失活和 NFE2L2/NRF2 激活。值得注意的是，BCR(KEAP1) 复合物将其泛素连接酶活性扩展到 SQSTM1/p62、BPTF 和 PGAM5 等底物，通过蛋白酶体调节它们的降解。BCR(KEAP1) 复合物的泛素连接酶活性因氧化应激和萝卜硫素等亲电代谢物而受到抑制，因为这些代谢物与 KEAP1 中的反应性半胱氨酸残基发生反应，导致非酶促共价修饰，从而使复合物丧失功能。此外，选择性自噬通过KEAP1和SQSTM1/p62之间的相互作用导致BCR(KEAP1)复合物失活，促进该复合物在包涵体中的隔离并促进其降解。
Measured by its ability to inhibit the proliferation of A549 cells. The ED50 for this effect is 1.117-2.321 μg/mL.
Greater than 85% as determined by reducing SDS-PAGE
Stored at -20°C for 2 years from date of receipt. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.