| 纯度 | > 90 % SDS-PAGE. |
| 种属 | Human |
| 靶点 | AKR1C3 |
| Uniprot No | P42330 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-323aa |
| 氨基酸序列 | MDSKHQCVKLNDGHFMPVLGFGTYAPPEVPRSKALEVTKLAIEAGFRHIDSAHLYNNEEQVGLAIRSKIADGSVKREDIFYTSKLWSTFHRPELVRPALENSLKKAQLDYVDLYLIHSPMSLKPGEELSPTDENGKVIFDIVDLCTTWEAMEKCKDAGLAKSIGVSNFNRRQLEMILNKPGLKYKPVCNQVECHPYFNRSKLLDFCKSKDIVLVAYSALGSQRDKRWVDPNSPVLLEDPVLCALAKKHKRTPALIALRYQLQRGVVVLAKSYNEQRIRQNVQVFEFQLTAEDMKAIDGLDRNLHYFNSDSFASHPNYPYSDEY |
| 预测分子量 | 43.8 kDa |
| 蛋白标签 | His tag N-Terminus |
| 缓冲液 | PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300. |
| 稳定性 & 储存条件 | Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt. Reconstituted protein solution can be stored at 2-8°C for 2-7 days. Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months. |
| 复溶 | Always centrifuge tubes before opening.Do not mix by vortex or pipetting. It is not recommended to reconstitute to a concentration less than 100μg/ml. Dissolve the lyophilized protein in distilled water. Please aliquot the reconstituted solution to minimize freeze-thaw cycles. |
以下是关于AKR1C3重组蛋白的3篇代表性文献及其摘要内容：
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1. **文献名称**: *"Structural and functional characterization of human recombinant AKR1C3"*
**作者**: Penning TM, et al.
**摘要**: 该研究通过重组表达纯化人源AKR1C3蛋白，分析了其酶活性及底物特异性，发现其在类固醇激素代谢(如孕酮和睾酮)中起关键作用，并探讨了其与肿瘤耐药性的潜在关联。
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2. **文献名称**: *"AKR1C3 as a target in castration-resistant prostate cancer: insights from recombinant enzyme studies"*
**作者**: Adeniji AO, et al.
**摘要**: 研究利用重组AKR1C3蛋白模型，揭示了其在去势抵抗性前列腺癌中通过催化雄激素前体转化为活性雄激素的机制，为开发AKR1C3抑制剂提供了生化依据。
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3. **文献名称**: *"Crystal structure of AKR1C3 in complex with inhibitors: implications for drug design"*
**作者**: Bylund J, et al.
**摘要**: 通过解析重组AKR1C3蛋白与多种抑制剂的复合物晶体结构，阐明了其活性位点特征，为设计高选择性抗癌药物(如针对白血病和实体瘤)提供了结构生物学基础。
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如需更多文献或具体领域(如疾病机制、抑制剂开发)，可进一步补充关键词优化检索。
AKR1C3 (aldo-keto reductase family 1 member C3) is a member of the aldo-keto reductase superfamily, a group of enzymes involved in steroidogenesis, prostaglandin metabolism, and detoxification of xenobiotics. This 37 kDa cytosolic protein, also known as type 5 17β-hydroxysteroid dehydrogenase, plays critical roles in hormone regulation by catalyzing NADPH-dependent reductions of ketosteroids, prostaglandins, and lipid peroxidation products. Its ability to convert weak androgens into more potent forms and regulate estrogen/androgen balance links it to numerous physiological and pathological processes.
In human physiology, AKR1C3 contributes to steroid hormone homeostasis, particularly in reproductive tissues, liver, and mammary glands. Pathologically, it has gained attention for its overexpression in hormone-dependent cancers (prostate, breast, endometrial), where it promotes cancer progression through androgen receptor activation and estrogen signaling modulation. It also mediates chemoresistance in leukemia and solid tumors by inactivating chemotherapeutic agents like doxorubicin and regulating oxidative stress responses.
Recombinant AKR1C3 protein, typically produced in E. coli or mammalian expression systems, retains the enzymatic properties of native protein while offering batch-to-batch consistency. Its production enables detailed biochemical characterization, inhibitor screening for anticancer drug development, and structural studies (X-ray crystallography revealed its TIM barrel fold with conserved cofactor-binding domain). Researchers utilize this tool to study substrate specificity, enzyme kinetics, and interactions with therapeutic inhibitors. Current applications extend to developing diagnostic biomarkers and targeted therapies, particularly for castration-resistant prostate cancer where AKR1C3-driven intracrine androgen synthesis remains a key therapeutic challenge.
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