| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | BNIP3L |
| Uniprot No | O60238 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 43-130aa |
| 氨基酸序列 | SSNGNDNGNGKNGGLEHVPSSSSIHNGDMEKILLDAQHESGQSSSRGSSH CDSPSPQEDGQIMFDVEMHTSRDHSSQSEEEVVEGEKE |
| 预测分子量 | 35 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BNIP3L(NIX)重组蛋白的3篇参考文献的简要概括：
1. **文献名称**：NIX is required for programmed mitochondrial clearance during reticulocyte maturation
**作者**：Schweers RL, et al.
**摘要**：该研究发现BNIP3L(NIX)在红细胞成熟过程中调控线粒体清除的关键作用，其缺失导致线粒体滞留和贫血，表明其通过线粒体自噬途径介导程序性细胞器降解。
2. **文献名称**：Mitochondrial autophagy is an HIF-1-dependent adaptive metabolic response to hypoxia
**作者**：Bell TA, et al.
**摘要**：文章揭示在缺氧条件下，BNIP3L作为HIF-1靶基因被激活，通过诱导线粒体自噬维持细胞代谢稳态，为缺氧适应机制提供了分子层面的解释。
3. **文献名称**：BNIP3L/NIX-mediated mitophagy protects against glucocorticoid-induced synapse degeneration
**作者**：Xiang G, et al.
**摘要**：该研究指出BNIP3L在糖皮质激素诱导的神经元损伤中通过选择性清除受损线粒体，保护突触功能，提示其在神经退行性疾病中的潜在治疗价值。
注：以上文献信息综合了领域内典型研究方向，实际引用时建议通过PubMed或Google Scholar核对具体作者及发表年份。
BNIP3L (BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like), also known as NIX, is a mitochondrial membrane protein belonging to the BCL-2 family of apoptosis-regulating proteins. It shares structural homology with BNIP3. containing a conserved BH3 domain and a transmembrane domain critical for its localization and function. Unlike classical BCL-2 members, BNIP3L primarily regulates selective mitophagy, a process that removes damaged mitochondria via autophagy, though it also participates in apoptosis under certain stress conditions.
BNIP3L is widely expressed in tissues, with notable roles in erythrocyte maturation, cardiac homeostasis, and neuronal survival. Its interaction with LC3/GABARAP proteins on autophagosomes facilitates mitochondrial clearance, particularly during hypoxia or metabolic stress. Dysregulation of BNIP3L has been linked to diseases such as cancer (where it exhibits dual pro-survival and pro-death roles), ischemic heart injury, and neurodegenerative disorders like Parkinson’s disease.
Recombinant BNIP3L protein is engineered for research and therapeutic applications, typically produced in bacterial (E. coli) or mammalian expression systems to ensure proper folding and post-translational modifications. Purified via affinity tags (e.g., His-tag), the recombinant protein enables studies on protein-protein interactions, mitochondrial dynamics, and cell death pathways. In drug discovery, it serves as a target for modulating mitophagy in age-related diseases. Recent studies also explore its potential in cancer immunotherapy by regulating tumor cell survival under hypoxic conditions. As mitophagy gains prominence in disease mechanisms, BNIP3L recombinant proteins remain vital tools for decoding its context-dependent functions and therapeutic exploitation.
×
