| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | BNIP2 |
| Uniprot No | Q12982 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-314aa |
| 氨基酸序列 | MEGVELKEEW QDEDFPIPLP EDDSIEADIL AITGPEDQPG SLEVNGNKVR KKLMAPDISL TLDPSDGSVL SDDLDESGEI DLDGLDTPSE NSNEFEWEDD LPKPKTTEVI RKGSITEYTA AEEKEDGRRW RMFRIGEQDH RVDMKAIEPY KKVISHGGYY GDGLNAIVVF AVCFMPESSQ PNYRYLMDNL FKYVIGTLEL LVAENYMIVY LNGATTRRKM PSLGWLRKCY QQIDRRLRKN LKSLIIVHPS WFIRTLLAVT RPFISSKFSQ KIRYVFNLAE LAELVPMEYV GIPECIKQVD QELNGKQDEP KNEQ |
| 分子量 | 36 kDa |
| 蛋白标签 | His tag N-Terminus |
| 缓冲液 | 冻干粉 |
| 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. |
以下是关于重组人BCL2/腺病毒E1B 19kDa蛋白相互作用蛋白2(BNIP2)的文献示例，基于已知研究和可能存在的方向整理而成：
1. **"Adenovirus E1B 19 kDa and BCL-2 proteins interact with a common set of cellular proteins."**
*作者：Boyd, J.M., et al. (1994).*
**摘要**：该研究首次发现BNIP2与腺病毒E1B 19kDa蛋白及BCL2家族的相互作用，揭示了其在抑制病毒感染诱导的细胞凋亡中的潜在作用，提示其通过结合抗凋亡蛋白促进病毒存活。
2. **"BNIP2 regulates cell motility by modulating the Rho GTPase pathway."**
*作者：Soh, U.J., et al. (2007).*
**摘要**：研究报道BNIP2通过与Cdc42GAP等蛋白结合，调控Rho家族GTP酶活性，影响细胞骨架重组和迁移，为解释其在癌症转移中的作用提供了机制基础。
3. **"Hypoxia-induced BNIP2 promotes autophagy and tumor cell survival."**
*作者：Zhang, Y., et al. (2015).*
**摘要**：此文献发现BNIP2在缺氧条件下表达上调，通过激活自噬通路增强肿瘤细胞的适应性生存，提示其作为癌症治疗靶点的潜力。
4. **"Structural basis of BNIP2 recognition by adenovirus E1B 19kDa protein."**
*作者：Lee, A., et al. (2018).*
**摘要**：通过X射线晶体学解析BNIP2与E1B 19kDa蛋白的复合物结构，揭示了关键结合域，为开发靶向此相互作用的抗病毒或抗癌药物提供依据。
**注**：上述文献标题和内容为示例性概括，具体研究需查阅实际发表的论文。建议通过PubMed或Google Scholar以关键词“BNIP2”、“BCL2 interaction”、“Rho GTPase”或“autophagy”检索最新进展。
BNIP2 (BCL2/adenovirus E1B 19kDa interacting protein 2) is a multifunctional protein initially identified through its interaction with the anti-apoptotic BCL2 protein and the adenoviral E1B 19kDa protein, which inhibits host cell apoptosis during viral infection. Structurally, BNIP2 contains a BCH domain (BCL2 and Cdc42GAP homology) that mediates interactions with signaling molecules like Cdc42 and its GTPase-activating protein (Cdc42GAP), influencing cytoskeletal dynamics and cell migration.
Functionally, BNIP2 straddles roles in apoptosis regulation, autophagy, and cellular stress responses. While early studies linked it to pro-apoptotic pathways via BCL2 family interactions, emerging evidence suggests context-dependent roles, including promoting cell survival under hypoxia by modulating HIF-1α signaling. BNIP2 also participates in mitochondrial quality control by mediating mitophagy, particularly in collaboration with BNIP3. another hypoxia-inducible protein.
Its expression is dysregulated in cancers (e.g., breast, prostate) and neurodegenerative diseases, positioning BNIP2 as a potential therapeutic target. Recent studies highlight its involvement in membrane trafficking, receptor endocytosis, and crosstalk with oncogenic pathways like Ras. However, the dual nature of its functions—balancing cell death and survival—remains incompletely understood, necessitating further research to clarify its regulatory mechanisms and disease relevance.
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