| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | MYBPC3 |
| Uniprot No | Q14896 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-328aa |
| 氨基酸序列 | MPEPGKKPVSAFSKKPRSVEVAAGSPAVFEAETERAGVKVRWQRGGSDIS ASNKYGLATEGTRHTLTVREVGPADQGSYAVIAGSSKVKFDLKVIEAEKA EPMLAPAPAPAEATGAPGEAPAPAAELGESAPSPKGSSSAALNGPTPGAP DDPIGLFVMRPQDGEVTVGGSITFSARVAGASLLKPPVVKWFKGKWVDLS SKVGQHLQLHDSYDRASKVYLFELHITDAQPAFTGSYRCEVSTKDKFDCS NFNLTVHEAMGTGDLDLLSAFRRTSLAGGGRRISDSHEDTGILDFSSLLK KRDSFRTPRDSKLEAPAEEDVWEILRQA |
| 预测分子量 | 51 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MYBPC3重组蛋白的3篇代表性文献示例(注：文献为假设性示例，实际引用需核实原文)：
1. **标题**：*"Recombinant MYBPC3 protein expression and functional analysis in cardiomyocytes"*
**作者**：Tardiff JC, et al.
**摘要**：研究利用大肠杆菌表达系统制备重组人源MYBPC3蛋白，分析其与肌球蛋白的相互作用，揭示其在心肌收缩调控中的结构域特异性功能。
2. **标题**：*"Pathogenic mutations disrupt MYBPC3 protein stability via altered phosphorylation"*
**作者**：Seidman CE, et al.
**摘要**：通过体外重组蛋白实验，证明肥厚型心肌病相关MYBPC3突变导致蛋白磷酸化异常，加速其蛋白酶体降解，破坏心肌细胞收缩稳态。
3. **标题**：*"Structural insights into MYBPC3-cardiac myosin complex by cryo-EM"*
**作者**：Morales RJ, et al.
**摘要**：采用冷冻电镜解析重组MYBPC3与心肌肌球蛋白的复合体结构，揭示其C端结构域在调节肌小节组装中的分子机制。
如需真实文献，建议通过PubMed或Google Scholar检索关键词“MYBPC3 recombinant protein”或结合具体研究领域筛选近年高引论文。
MYBPC3 recombinant protein is derived from the MYBPC3 gene, which encodes cardiac myosin-binding protein C (cMyBP-C), a key regulatory component of the sarcomere in cardiomyocytes. This protein plays a critical role in maintaining the structural integrity of cardiac muscle and modulating contractile function through interactions with myosin, actin, and titin. Mutations in MYBPC3 are strongly associated with hypertrophic cardiomyopathy (HCM), a common inherited cardiac disorder characterized by left ventricular hypertrophy, arrhythmias, and an increased risk of sudden cardiac death. Approximately 50% of HCM cases are linked to MYBPC3 mutations, often resulting in truncated or misfolded proteins that disrupt sarcomere organization and calcium signaling.
Recombinant MYBPC3 protein is typically produced using heterologous expression systems, such as *E. coli* or mammalian cell cultures, to study its structure-function relationships, post-translational modifications (e.g., phosphorylation), and pathogenic mechanisms. Researchers utilize this protein to investigate how mutations impair its ability to stabilize the sarcomere or regulate cross-bridge cycling during contraction. It also serves as a tool for developing therapeutic strategies, including small-molecule drugs or gene-editing approaches (e.g., CRISPR-Cas9) aimed at restoring normal protein expression or function. Additionally, recombinant MYBPC3 is used in diagnostic assays to identify autoantibodies in HCM patients and to screen potential compounds targeting MYBPC3-related pathways. Its study has advanced understanding of cardiac biomechanics and the molecular basis of HCM, offering insights into precision medicine for genetic heart diseases.
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