| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | PIK3Ca |
| Uniprot No | P42336 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 797-1068aa |
| 氨基酸序列 | NEIIFKNGDDLRQDMLTLQIIRIMENIWQNQGLDLRMLPYGCLSIGDCVGLIEVVRNSHTIMQIQCKGGLKGALQFNSHTLHQWLKDKNKGEIYDAAIDLFTRSCAGYCVATFILGIGDRHNSNIMVKDDGQLFHIDFGHFLDHKKKKFGYKRERVPFVLTQDFLIVISKGAQECTKTREFERFQEMCYKAYLAIRQHANLFINLFSMMLGSGMPELQSFDDIAYIRKTLALDKTEQEALEYFMKQMNDAHHGGWTTKMDWIFHTIKQHALN |
| 预测分子量 | 33.9 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PIK3CA重组蛋白的3篇代表性文献，涵盖结构、功能及药物开发研究：
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1. **文献名称**：*Oncogenic Mutations in PIK3CA Disrupt Regulatory Interactions with the p85α Subunit*
**作者**：Mandelker, D. et al.
**摘要**：通过晶体结构分析，揭示了PIK3CA致癌突变(如H1047R)如何破坏其与调控亚基p85α的相互作用，导致PI3Kα组成性激活，促进肿瘤发生。
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2. **文献名称**：*Functional Analysis of PIK3CA Mutations in Human Cancer*
**作者**：Ikenoue, T. et al.
**摘要**：研究发现常见PIK3CA突变体(如E545K和H1047R)的重组蛋白具有显著增强的激酶活性，并证实其通过激活Akt/mTOR通路驱动细胞转化和肿瘤生长。
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3. **文献名称**：*Structure-Based Drug Design Identifies a Selective Inhibitor of Mutant PIK3CA*
**作者**：Furet, P. et al.
**摘要**：利用重组突变型PIK3CA蛋白的晶体结构，开发出选择性抑制剂Alpelisib(BYL719)，阐明其通过靶向突变诱导的变构位点抑制酶活性，为临床治疗提供依据。
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这些研究从分子机制到转化应用，系统解析了PIK3CA重组蛋白的功能及靶向策略。如需扩展，可进一步查阅PI3Kα结构生物学或临床试验相关论文。
**Background of PIK3CA Recombinant Protein**
The PIK3CA gene encodes the catalytic alpha subunit (p110α) of phosphatidylinositol 3-kinase (PI3K), a lipid kinase central to the PI3K/AKT/mTOR signaling pathway. This pathway regulates critical cellular processes, including growth, survival, metabolism, and proliferation. PIK3CA is a member of the class I PI3K family, which functions as a heterodimer composed of a catalytic subunit (p110α) and a regulatory subunit (p85). Activation typically occurs via receptor tyrosine kinases (RTKs) or G-protein-coupled receptors (GPCRs), leading to the conversion of phosphatidylinositol-4.5-bisphosphate (PIP2) to phosphatidylinositol-3.4.5-trisphosphate (PIP3), a secondary messenger that recruits downstream effectors like AKT.
Structurally, p110α contains multiple domains: an adaptor-binding domain (ABD) for p85 interaction, a Ras-binding domain (RBD), a C2 domain, a helical domain, and a catalytic kinase domain. Mutations in PIK3CA, particularly in the helical (E542K, E545K) and kinase (H1047R) domains, are oncogenic drivers in cancers such as breast, colorectal, and endometrial tumors. These gain-of-function mutations hyperactivate PI3K signaling, promoting uncontrolled cell growth and therapy resistance.
Recombinant PIK3CA protein is engineered in vitro using expression systems (e.g., mammalian, insect cells) to retain post-translational modifications and functional activity. It serves as a vital tool for studying PI3K biology, screening inhibitors (e.g., Alpelisib), elucidating mutation-specific mechanisms, and developing targeted therapies. Its use in structural studies (e.g., cryo-EM) has advanced understanding of PI3Kα activation and inhibitor binding, guiding precision oncology efforts.
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