| 纯度 | >95%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篇参考文献及其摘要概括：
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1. **文献名称**：*"A mutation in the glycerol-3-phosphate dehydrogenase 1-like (GPD1L) gene causes Brugada syndrome"*
**作者**：London, B. 等 (2007)
**摘要**：该研究首次发现GPD1L基因突变与Brugada综合征(一种致死性心律失常)相关。通过体外重组蛋白实验，表明突变导致GPD1L蛋白功能异常，进而影响心脏钠离子通道(SCN5A)的活性，诱发心律失常。
2. **文献名称**：*"GPD1L links redox-dependent regulation of SCN5A to sudden death syndromes"*
**作者**：Valdivia, C.R. 等 (2009)
**摘要**：研究揭示了GPD1L通过调控心脏钠通道SCN5A的氧化还原状态维持正常功能。利用重组GPD1L蛋白，发现其与SCN5A直接互作，并在缺氧条件下通过减少活性氧(ROS)保护通道功能，突变则导致通道失活异常。
3. **文献名称**：*"GPD1L inhibits adipogenesis via suppression of PPARγ activity"*
**作者**：Harada, N. 等 (2012)
**摘要**：该研究通过表达重组GPD1L蛋白，证明其通过抑制过氧化物酶体增殖物激活受体γ(PPARγ)的转录活性，负向调控脂肪细胞分化，提示GPD1L在代谢性疾病中的潜在作用。
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**备注**：上述文献聚焦于GPD1L在心脏电生理、氧化应激调控及代谢中的功能，均涉及重组蛋白技术验证机制。如需具体期刊卷页或补充文献，可进一步提供方向细化。
Glycerol-3-phosphate dehydrogenase 1-like (GPD1L) is a protein encoded by the *GPD1L* gene in humans, located on chromosome 3p22.3. It shares structural homology with glycerol-3-phosphate dehydrogenase (GPD1), a key enzyme in the glycerol phosphate shuttle that links glycolysis and lipid metabolism. However, GPD1L lacks intrinsic enzymatic activity due to amino acid substitutions in its catalytic domain. Instead, it plays a regulatory role in cellular processes, particularly in cardiac ion channel function. Research has linked GPD1L mutations to Brugada syndrome, a rare inherited arrhythmia disorder characterized by abnormal electrocardiogram (ECG) patterns and an increased risk of sudden cardiac death. Specifically, GPD1L interacts with the cardiac sodium channel Nav1.5 (encoded by *SCN5A*), modulating its trafficking and function. Mutations in *GPD1L* disrupt this interaction, leading to reduced sodium current (INa) and altered cardiac excitability.
Recombinant GPD1L protein is produced using expression systems like *E. coli* or mammalian cells, enabling functional studies. Its purification often involves affinity tags (e.g., His-tag) for ease of isolation. Studies using recombinant GPD1L have clarified its role in redox regulation, as it may influence Nav1.5 activity through cysteine residues sensitive to oxidative stress. Additionally, recombinant protein tools aid in mapping interaction domains with Nav1.5 and screening potential therapeutic compounds targeting Brugada syndrome. Structural analyses (e.g., X-ray crystallography) of recombinant GPD1L provide insights into its conformation and mutation-induced dysfunction. Beyond cardiology, GPD1L is implicated in cancer and metabolic diseases, though these roles remain less explored. Overall, recombinant GPD1L serves as a vital reagent for dissecting molecular mechanisms in arrhythmogenesis and developing precision therapies for channelopathies.
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