| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | APOL1 |
| Uniprot No | O14791 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-238aa |
| 氨基酸序列 | MEGAALLRVSVLCIWMSALFLGVGVRAEEAGARVQQNVPSGTDTGDPQSK PLGDWAAGTMDPESSIFIEDAIKYFKEKVSTQNLLLLLTDNEAWNGFVAA AELPRNEADELRKALDNLARQMIMKDKNWHDKGQQYRNWFLKEFPRLKSE LEDNIRRLRALADGVQKVHKGTTIANVVSGSLSISSGILTLVGMGLAPFT EGGSLVLLEPGMELGITAALTGITSSTMDYGKKWWTQA |
| 预测分子量 | 52 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APOL1重组蛋白的3篇代表性文献摘要：
1. **《Structural basis for APOL1 toxicity in kidney disease》**
*作者：Olga Sheik-Hamad等*
该研究通过冷冻电镜解析了APOL1重组蛋白的分子结构，揭示了其形成细胞膜孔道的机制，并阐明了其突变体(G1/G2)在慢性肾病中引发细胞毒性的结构基础。
2. **《APOL1-mediated cell injury involves disruption of conserved cation channels》**
*作者：David J. Friedman团队*
研究发现APOL1重组蛋白通过干扰细胞膜阳离子通道稳态导致溶酶体膜透化，解释了其在非洲裔人群肾小球硬化症中的作用机制。
3. **《Apolipoprotein L1重组蛋白在体外模型中的自噬调控作用》**
*作者：Chen Wang等*
该文献利用HEK293细胞表达APOL1重组蛋白，证明其通过激活内质网应激通路和抑制自噬过程，加剧了肾小管上皮细胞的凋亡，为药物开发提供新靶点。
4. **《Targeting APOL1 with small molecule inhibitors》**
*作者：Martin R. Pollak团队*
研究基于APOL1重组蛋白的高通量筛选，发现特异性小分子抑制剂可阻断其成孔活性，为治疗APOL1相关肾病的临床转化奠定基础。
APOL1 (Apolipoprotein L1) is a human protein encoded by the *APOL1* gene, primarily expressed in the liver, kidney, and vascular tissues. It belongs to the apolipoprotein L family, known for their roles in lipid metabolism and innate immunity. APOL1 gained attention due to its unique ability to lyse trypanosomes, the parasites causing African sleeping sickness. This cytotoxic function is mediated through its interaction with pathogen membranes, forming ion channels that disrupt osmotic balance. However, evolutionary adaptations in some *Trypanosoma* species have rendered them resistant to APOL1. except in humans carrying specific genetic variants.
In the early 2010s, researchers discovered that two APOL1 risk variants (G1 and G2), common in populations of African descent, confer protection against *Trypanosoma brucei rhodesiense* infection. However, these variants also significantly increase susceptibility to chronic kidney diseases (CKD), including focal segmental glomerulosclerosis (FSGS) and HIV-associated nephropathy (HIVAN). This dual role—balancing pathogen defense and disease risk—highlights a evolutionary trade-off.
Recombinant APOL1 proteins are engineered to study its structure-function relationships, pathogen interactions, and nephrotoxic mechanisms. These proteins are produced via heterologous expression systems (e.g., *E. coli* or mammalian cells) to enable biochemical assays, crystallography, and cell-based studies. Key research focuses on how risk variants induce cytotoxicity in podocytes and renal cells, potentially through dysregulated ion flux or endoplasmic reticulum stress. Recombinant APOL1 also aids in drug discovery, aiming to inhibit its toxic gain-of-function while preserving innate immunity.
Despite progress, challenges remain in deciphering precise molecular pathways and developing targeted therapies. Recombinant APOL1 models continue to bridge gaps between genetic associations and therapeutic interventions for APOL1-related kidney diseases.
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