| 纯度 | > 90 % SDS-PAGE. |
| 种属 | Human |
| 靶点 | Bcl2L |
| Uniprot No | Q07817 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-209aa |
| 氨基酸序列 | MSQSNRELVVDFLSYKLSQKGYSWSQFSDVEENRTEAPEGTESEMETPSAINGNPSWHLADSPAVNGATGHSSSLDAREVIPMAAVKQALREAGDEFELRYRRAFSDLTSQLHITPGTAYQSFEQVVNELFRDGVNWGRIVAFFSFGGALCVESVDKEMQVLVSRIAAWMATYLNDHLEPWIQENGGWDTFVELYGNNAAAESRKGQER |
| 预测分子量 | 39.4kDa |
| 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Bcl2L(Bcl-xL)重组蛋白的3篇文献摘要示例(文献标题与内容为虚构模拟，供参考)：
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1. **文献名称**：*Structural Basis of Bcl-xL Recombinant Protein Interaction with Pro-apoptotic BH3 Peptides*
**作者**：Chen L, et al.
**摘要**：本研究通过重组表达纯化Bcl-xL蛋白，结合X射线晶体学解析其与BH3结构域肽段的复合物结构，揭示了Bcl-xL抗凋亡作用的关键结合位点，为靶向药物设计提供结构基础。
2. **文献名称**：*Optimized Expression and Purification of Recombinant Bcl-xL in E. coli for Functional Studies*
**作者**：Smith J, et al.
**摘要**：报道了一种高效的大肠杆菌表达系统，通过优化诱导条件和纯化步骤(如亲和层析)获得高纯度、高活性的重组Bcl-xL蛋白，验证其抑制细胞凋亡的生物学功能。
3. **文献名称**：*Recombinant Bcl-xL Protein Modulates Mitochondrial Membrane Permeability in Cancer Cells*
**作者**：Wang Y, et al.
**摘要**：利用重组Bcl-xL蛋白研究其对线粒体膜通透性的调控机制，发现其通过结合Bax蛋白抑制细胞色素C释放，从而阻止癌细胞凋亡，提示其在肿瘤耐药性中的作用。
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如需真实文献，建议通过PubMed或Google Scholar搜索关键词“recombinant Bcl-xL protein”或“Bcl2L1 recombinant expression”获取。
Bcl2L (Bcl-2-like) recombinant protein is derived from the Bcl-2 family of proteins, which are critical regulators of apoptosis (programmed cell death). The Bcl-2 family includes both anti-apoptotic (e.g., Bcl-2. Bcl-xL, Mcl-1) and pro-apoptotic members (e.g., Bax, Bak, Bid). Bcl2L, often referred to as Bcl-xL, is a key anti-apoptotic protein that promotes cell survival by inhibiting mitochondrial outer membrane permeabilization (MOMP), a pivotal step in the intrinsic apoptotic pathway. It achieves this by binding and neutralizing pro-apoptotic factors like Bax and Bak, thereby preventing cytochrome c release and subsequent caspase activation.
Bcl-xL is encoded by the *BCL2L1* gene, which undergoes alternative splicing to produce two isoforms: the long isoform (Bcl-xL) and a short pro-apoptotic isoform (Bcl-xS). Its expression is prevalent in various tissues, particularly in cancers, where its overexpression is linked to tumor progression, resistance to chemotherapy, and poor prognosis. This has made Bcl-xL a therapeutic target; inhibitors like ABT-263 (navitoclax) have been developed to disrupt its interaction with pro-apoptotic proteins.
Recombinant Bcl2L proteins are engineered for research and preclinical applications. They are typically produced in *E. coli* or mammalian expression systems, ensuring proper folding and post-translational modifications. These recombinant proteins are used to study apoptosis mechanisms, screen small-molecule inhibitors, and validate drug-target interactions. In disease models, they help elucidate how cancer cells evade apoptosis or how neuroprotective signals operate in neurodegenerative disorders. Structural studies of recombinant Bcl-xL have also revealed binding sites for partners and inhibitors, guiding rational drug design. However, its dual role in survival and potential toxicity in normal cells underscores the complexity of targeting Bcl-xL therapeutically.
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