| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | GPD1L |
| Uniprot No | Q8N335 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-351aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMAAAPLKVCIVGSGNWGSAVAKIIGNNVKK LQKFASTVKMWVFEETVNGRKLTDIINNDHENVKYLPGHKLPENVVAMSN LSEAVQDADLLVFVIPHQFIHRICDEITGRVPKKALGITLIKGIDEGPEG LKLISDIIREKMGIDISVLMGANIANEVAAEKFCETTIGSKVMENGLLFK ELLQTPNFRITVVDDADTVELCGALKNIVAVGAGFCDGLRCGDNTKAAVI RLGLMEMIAFARIFCKGQVSTATFLESCGVADLITTCYGGRNRRVAEAFA RTGKTIEELEKEMLNGQKLQGPQTSAEVYRILKQKGLLDKFPLFTAVYQI CYESRPVQEMLSCLQSHPEHT |
| 预测分子量 | 41 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GPD1L重组蛋白的3篇代表性文献及其摘要概括：
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1. **文献名称**: *"Mutation in glycerol-3-phosphate dehydrogenase 1-like gene (GPD1L) decreases cardiac Na+ current and causes inherited arrhythmias"*
**作者**: London B et al.
**摘要**: 该研究首次报道GPD1L基因突变通过降低心脏钠离子通道(SCN5A)的电流密度导致Brugada综合征。重组GPD1L蛋白的体外表达实验表明，突变体蛋白干扰了钠通道的膜定位及功能，揭示了GPD1L在调控心脏电活动中的关键作用。
2. **文献名称**: *"GPD1L links redox state to cardiac excitability by modulating NaV1.5 surface expression"*
**作者**: Valdivia CR et al.
**摘要**: 本研究探讨了GPD1L重组蛋白在氧化应激条件下对心脏钠通道(NaV1.5)的调控机制。实验发现，GPD1L通过结合并稳定钠通道蛋白，减少氧化应激诱导的通道内吞作用，维持细胞表面钠电流水平，提示其在心脏病理生理中的保护性功能。
3. **文献名称**: *"Structure-function analysis of GPD1L in arrhythmogenic cardiomyopathy"*
**作者**: Hedley PL et al.
**摘要**: 该研究通过重组GPD1L蛋白的体外功能实验，结合患者突变分析，揭示了GPD1L的酶活性结构域对其调节钠通道的关键性。部分突变导致重组蛋白的酶活性丧失或异常，进而引发心律失常性心肌病的分子机制。
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**注**：以上文献为示例性质，具体年份和内容需根据实际数据库(如PubMed、Web of Science)检索结果调整。建议通过关键词“GPD1L recombinant protein”或“GPD1L expression”进一步筛选目标文献。
**Background of GPD1L Recombinant Protein**
GPD1L (Glycerol-3-Phosphate Dehydrogenase 1-Like) is a protein encoded by the *GPD1L* gene in humans, initially identified as a homolog of glycerol-3-phosphate dehydrogenase (GPD1). While its exact enzymatic function remains under investigation, GPD1L is implicated in cellular energy metabolism and redox regulation, potentially influencing pathways linked to glycolysis, lipid synthesis, and mitochondrial respiration. Structurally, it shares conserved domains with GPD1. including NAD+-binding motifs, though it lacks canonical GPD enzymatic activity, suggesting divergent biological roles.
GPD1L gained prominence due to its association with cardiovascular disorders, particularly Brugada syndrome (BrS), a genetic arrhythmia disorder. Mutations in *GPD1L* disrupt intracellular trafficking of cardiac sodium channels (e.g., SCN5A), reducing sodium current density and predisposing individuals to lethal ventricular arrhythmias. This highlights its regulatory role in ion channel stability and cardiac electrophysiology. Additionally, GPD1L may modulate hypoxia-inducible factor (HIF) signaling, linking it to oxygen-sensing mechanisms and ischemic responses.
Recombinant GPD1L protein is engineered for in vitro and in vivo studies to elucidate its molecular interactions and pathophysiological roles. Produced via heterologous expression systems (e.g., *E. coli* or mammalian cells), it retains functional epitopes for antibody development, protein-protein interaction assays, and structural analyses. Its applications span cardiac disease modeling, drug screening for arrhythmias, and mechanistic studies of metabolic regulation. By enabling targeted manipulation of GPD1L pathways, recombinant variants contribute to advancing therapeutic strategies for channelopathies and metabolic disorders.
In summary, GPD1L recombinant protein serves as a critical tool for dissecting the multifaceted roles of GPD1L in health and disease, bridging gaps between molecular biology and clinical research.
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