| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ABCC8 |
| Uniprot No | Q09428 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 611-710aa |
| 氨基酸序列 | SEFLSSAEIREEQCAPHEPTPQGPASKYQAVPLRVVNRKRPAREDCRGLT GPLQSLVPSADGDADNCCVQIMGGYFTWTPDGIPTLSNITIRIPRGQLTM |
| 预测分子量 | 37 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ABCC8重组蛋白的3篇代表性文献摘要示例：
1. **"Structural insights into ABCC8-mediated ATP-sensitive potassium channel regulation"**
*作者：Martin et al. (2021)*
摘要：通过冷冻电镜解析ABCC8(SUR1)重组蛋白与KIR6.2通道复合体的三维结构，揭示ATP结合与通道门控的分子机制，为糖尿病药物设计提供依据。
2. **"Functional reconstitution of human ABCC8/SUR1 in lipid bilayers reveals sulfonylurea sensitivity"**
*作者：Aguilar-Bryan et al. (1995)*
摘要：首次成功在体外重组表达ABCC8蛋白并重构功能完整的KATP通道，验证其磺酰脲类药物(如格列本脲)的特异性抑制作用。
3. **"ABCC8 mutations impair glucose-dependent insulin secretion via altered SUR1 protein stability"**
*作者：Ashcroft et al. (2005)*
摘要：研究先天性高胰岛素血症相关的ABCC8突变对重组蛋白稳定性的影响，揭示内质网滞留导致通道功能缺失的病理机制。
4. **"High-throughput screening of ABCC8 modulators using recombinant SUR1-expressing cell models"**
*作者：Zhang et al. (2020)*
摘要：开发基于ABCC8重组蛋白的细胞筛选平台，鉴定新型KATP通道开放剂，为糖尿病和神经保护药物开发提供候选分子。
注：以上文献为示例，实际引用需根据具体研究需求核实原文。
**Background of ABCC8 Recombinant Protein**
ABCC8 (ATP-binding cassette subfamily C member 8) is a gene encoding the sulfonylurea receptor 1 (SUR1), a regulatory subunit of the ATP-sensitive potassium (KATP) channel. This channel, primarily expressed in pancreatic β-cells and neurons, plays a critical role in coupling cellular metabolic status to membrane excitability. In β-cells, KATP channels regulate insulin secretion by sensing intracellular ATP/ADP levels, closing in response to high glucose to trigger insulin release.
Mutations in ABCC8 are linked to congenital hyperinsulinism (CHI) and neonatal diabetes. Loss-of-function mutations cause persistent insulin secretion despite hypoglycemia (CHI), while gain-of-function mutations impair insulin release, leading to diabetes. ABCC8 is also a pharmacologic target for sulfonylureas, oral antidiabetic drugs that bind SUR1 to stimulate insulin secretion.
Recombinant ABCC8 protein is produced via genetic engineering in systems like mammalian cells or bacteria, enabling studies on its structure, function, and interaction with drugs. It aids in deciphering mutation-specific mechanisms, screening therapeutic compounds, and understanding KATP channel dynamics. Its applications extend to developing personalized treatments for diabetes and CHI, as well as exploring neurologic roles due to its expression in the brain.
Overall, ABCC8 recombinant protein serves as a vital tool for both basic research and clinical translation in metabolic disorders.
×
