| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | cTnI |
| Uniprot No | O75914 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-559aa |
| 氨基酸序列 | MSDGLDNEEK PPAPPLRMNS NNRDSSALNH SSKPLPMAPE EKNKKARLRS IFPGGGDKTN KKKEKERPEI SLPSDFEHTI HVGFDAVTGE FTPDLYGSQM CPGKLPEGIP EQWARLLQTS NITKLEQKKN PQAVLDVLKF YDSKETVNNQ KYMSFTSGDK SAHGYIAAHP SSTKTASEPP LAPPVSEEED EEEEEEEDEN EPPPVIAPRP EHTKSIYTRS VVESIASPAV PNKEVTPPSA ENANSSTLYR NTDRQRKKSK MTDEEILEKL RSIVSVGDPK KKYTRFEKIG QGASGTVYTA LDIATGQEVA IKQMNLQQQP KKELIINEIL VMRENKNPNI VNYLDSYLVG DELWVVMEYL AGGSLTDVVT ETCMDEGQIA AVCRECLQAL DFLHSNQVIH RDIKSDNILL GMDGSVKLTD FGFCAQITPE QSKRSTMVGT PYWMAPEVVT RKAYGPKVDI WSLGIMAIEM VEGEPPYLNE NPLRALYLIA TNGTPELQNP ERLSAVFRDF LNRCLEMDVD RRGSAKELLQ HPFLKLAKPL SSLTPLIIAA KEAIKNSSR |
| 预测分子量 | 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cTnI(心肌肌钙蛋白I)重组蛋白的3篇模拟参考文献示例，涵盖表达、应用及结构研究：
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1. **文献名称**：*Expression and Purification of Recombinant Human Cardiac Troponin I in Escherichia coli for Immunoassay Development*
**作者**：Smith A, et al.
**摘要**：研究通过大肠杆菌表达系统高效表达重组人cTnI，优化了可溶性蛋白的纯化工艺，验证其与临床单克隆抗体的结合活性，为心肌梗死诊断试剂的开发提供标准品。
2. **文献名称**：*Structural and Functional Characterization of a Stable Mutant Recombinant cTnI for Cardiac Disease Modeling*
**作者**：Lee J, et al.
**摘要**：通过定点突变增强重组cTnI的稳定性，利用圆二色谱和分子动力学模拟分析其结构特征，并验证其在心肌缺血模型中的功能，为药物靶点研究提供工具。
3. **文献名称**：*Mammalian Cell-Derived Recombinant cTnI as a Reference Material in High-Sensitivity Clinical Assays*
**作者**：Garcia R, et al.
**摘要**：采用HEK293细胞表达重组cTnI，实现接近天然构象的翻译后修饰，验证其作为高灵敏度检测标准品的可靠性，提升临床检测一致性。
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以上文献示例聚焦不同技术路径(原核/真核表达)和应用场景(诊断、药物开发)，用户可根据实际研究方向调整关键词检索PubMed或Web of Science获取真实文献。
Cardiac troponin I (cTnI) is a regulatory protein exclusively expressed in cardiomyocytes, playing a critical role in cardiac muscle contraction. As a subunit of the troponin complex, cTnI interacts with troponin T (cTnT) and troponin C (cTnC) to regulate calcium-dependent actin-myosin interactions during the cardiac cycle. Its cardiac-specific isoform, distinct from skeletal muscle isoforms, makes it a gold-standard biomarker for diagnosing myocardial injury, particularly acute myocardial infarction.
Recombinant cTnI proteins are engineered using genetic engineering techniques to replicate the native human cTnI structure. These proteins are typically produced in heterologous expression systems, such as *E. coli* (prokaryotic) or mammalian cell lines (eukaryotic), to ensure proper post-translational modifications or high-yield production. The recombinant protein retains key functional domains, including the inhibitory peptide region (residues 1-30) and the mobile domain (residues 31-110), which are essential for antibody recognition in diagnostic assays.
The development of recombinant cTnI has addressed critical challenges in clinical diagnostics, including batch consistency and standardization of cardiac biomarker assays. It serves as a calibrator or control material in immunoassays, enabling accurate quantification of cTnI in patient samples. Additionally, recombinant cTnI is vital for research applications, such as studying cardiac pathophysiology, developing therapeutic antibodies, and validating detection platforms. Its use has significantly improved the sensitivity and specificity of cardiac testing, supporting early intervention in acute coronary syndromes. Ongoing advancements aim to optimize stability, minimize degradation-prone regions (e.g., N-terminal instability), and mimic post-translational modifications observed in circulating forms during myocardial injury.
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