| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | MYL3 |
| Uniprot No | P08590 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-195aa |
| 氨基酸序列 | MAPKKPEPKKDDAKAAPKAAPAPAPPPEPERPKEVEFDASKIKIEFTPEQIEEFKEAFMLFDRTPKCEMKITYGQCGDVLRALGQNPTQAEVLRVLGKPRQEELNTKMMDFETFLPMLQHISKNKDTGTYEDFVEGLRVFDKEGNGTVMGAELRHVLATLGERLTEDEVEKLMAGQEDSNGCINYEAFVKHIMSS |
| 预测分子量 | 48.8kDa |
| 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MYL3重组蛋白的3篇参考文献示例(注：以下内容为模拟虚构，实际文献需通过学术数据库查询)：
1. **文献名称**: *"Expression and Functional Characterization of Recombinant Human MYL3 in Cardiomyopathy Models"*
**作者**: Zhang L, et al.
**摘要**: 研究通过大肠杆菌系统成功表达并纯化重组人MYL3蛋白，验证其在体外心肌细胞收缩功能中的作用，发现MYL3突变可能导致肥厚型心肌病的病理机制。
2. **文献名称**: *"Structural Insights into MYL3 Interactions with Cardiac Myosin Heavy Chain"*
**作者**: Tanaka K, et al.
**摘要**: 利用X射线晶体学解析了重组MYL3蛋白与心肌肌球蛋白重链的结合结构，揭示了其调控心脏收缩的关键氨基酸残基及分子机制。
3. **文献名称**: *"Development of a MYL3 Recombinant Protein-Based Diagnostic Assay for Familial Hypertrophic Cardiomyopathy"*
**作者**: Gupta R, et al.
**摘要**: 构建了基于重组MYL3蛋白的ELISA检测方法，用于筛查家族性肥厚型心肌病患者中MYL3基因突变携带者，具有高灵敏度和特异性。
建议通过PubMed或Web of Science以“MYL3 recombinant protein”为关键词检索真实文献。
MYL3. also known as myosin light chain 3. is a regulatory protein critical for muscle contraction in cardiac and skeletal tissues. It belongs to the myosin light chain family, which modulates the ATPase activity of myosin heavy chains and influences the mechanical function of muscle fibers. Specifically, MYL3 is expressed predominantly in slow-twitch skeletal muscles and cardiac muscle, where it binds to the neck region of myosin heads in the thick filaments of sarcomeres. This interaction stabilizes myosin structure and fine-tunes contractile force generation in response to calcium signaling.
Recombinant MYL3 protein is produced using expression systems like *E. coli* or mammalian cell lines to mimic native post-translational modifications, such as phosphorylation. These modifications are essential for its functional role in regulating actin-myosin cross-bridge cycling. Research has linked MYL3 mutations to inherited cardiomyopathies, including hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM), where altered MYL3 function disrupts sarcomere organization and contractility.
In biomedical studies, recombinant MYL3 serves as a tool to investigate disease mechanisms, screen therapeutic compounds, and validate gene-editing strategies. It enables structural analyses (e.g., cryo-EM) to visualize how mutations impair myosin dynamics. Additionally, the protein aids in developing cellular models to test precision therapies targeting MYL3-related pathways. Its role in cardiac-specific contractility also positions it as a potential biomarker for heart disease diagnostics. Ongoing research focuses on leveraging recombinant MYL3 to bridge molecular insights with clinical applications, advancing treatments for muscle-related disorders.
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