| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | BNIP3 |
| Uniprot No | Q12983 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-194aa |
| 氨基酸序列 | MSQNGAPGMQEESLQGSWVELHFSNNGNGGSVPASVSIYNGDMEKILLDAQHESGRSSSK SSHCDSPPRSQTPQDTNRASETDTHSIGEKNSSQSEEDDIERRKEVESILKKNSDWIWDW SSRPENIPPKEFLFKHPKRTATLSMRNTSVMKKGGIFSAEFLKVFLPSLLLSHLLAIGLG IYIGRRLTTSTSTF |
| 预测分子量 | 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BNIP3重组蛋白的3篇参考文献及其摘要内容：
1. **文献名称**：*BNIP3 and genetic control of mitochondrial-mediated cell death*
**作者**：Vande Velde, C., et al.
**摘要**：该研究阐明了BNIP3重组蛋白通过靶向线粒体膜，激活线粒体自噬和细胞凋亡的分子机制，揭示了其结构域在促死亡信号中的关键作用。
2. **文献名称**：*Regulation of mitochondrial autophagy by hypoxia-inducible BNIP3*
**作者**：Zhang, H., et al.
**摘要**：文章证明缺氧条件下BNIP3重组蛋白表达上调，通过破坏线粒体膜完整性诱导选择性自噬，并探讨其与HIF-1信号通路的关联。
3. **文献名称**：*Functional analysis of BNIP3 in cancer cells using recombinant protein*
**作者**：Graham, R.M., et al.
**摘要**：研究利用重组BNIP3蛋白在肿瘤模型中验证其促凋亡功能，发现其通过ROS依赖性途径增强化疗敏感性，提示潜在治疗应用价值。
BNIP3 (Bcl-2/adenovirus E1B 19 kDa-interacting protein 3) is a mitochondrial membrane-associated protein belonging to the pro-apoptotic BH3-only subgroup of the Bcl-2 family. Initially identified for its role in apoptosis, BNIP3 is regulated by hypoxia-inducible factor 1α (HIF-1α) under low-oxygen conditions, linking it to cellular responses in ischemic or tumor microenvironments. Unlike canonical Bcl-2 proteins, BNIP3 induces apoptosis through a caspase-independent pathway, involving mitochondrial dysfunction and reactive oxygen species (ROS) generation. Beyond apoptosis, BNIP3 is a key mediator of mitophagy, selectively targeting damaged mitochondria for autophagic degradation, thereby maintaining mitochondrial quality and cellular homeostasis.
Structurally, BNIP3 contains a C-terminal transmembrane domain essential for mitochondrial localization and a N-terminal BH3 domain that facilitates interactions with anti-apoptotic proteins like Bcl-2 and Bcl-xL. However, its mitophagy function relies on interactions with LC3/GABARAP proteins via a conserved LIR (LC3-interacting region) motif. Dysregulation of BNIP3 is implicated in cancer, cardiovascular diseases, and neurodegenerative disorders, where altered expression correlates with tumor progression, cardiomyocyte death, or impaired mitochondrial clearance.
Recombinant BNIP3 proteins are typically produced using bacterial or mammalian expression systems to study its biochemical and functional properties. These proteins enable in vitro exploration of BNIP3’s dual roles in apoptosis and mitophagy, including binding assays, structural analyses, and mechanistic studies. Researchers also utilize recombinant BNIP3 to develop therapeutic strategies targeting hypoxia-related diseases or mitochondrial dysfunction. Its versatility as a molecular tool underscores its importance in deciphering cellular stress responses and designing targeted interventions.
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