纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | BCL2L13 |
Uniprot No | Q9BXK5 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 1-485aa |
氨基酸序列 | MASSSTVPLGFHYETKYVVLSYLGLLSQEKLQEQHLSSPQGVQLDIASQSLDQEILLKVKTEIEEELKSLDKEISEAFTSTGFDRHTSPVFSPANPESSMEDCLAHLGEKVSQELKEPLHKALQMLLSQPVTYQAFRECTLETTVHASGWNKILVPLVLLRQMLLELTRRGQEPLSALLQFGVTYLEDYSAEYIIQQGGWGTVFSLESEEEEYPGITAEDSNDIYILPSDNSGQVSPPESPTVTTSWQSESLPVSLSASQSWHTESLPVSLGPESWQQIAMDPEEVKSLDSNGAGEKSENNSSNSDIVHVEKEEVPEGMEEAAVASVVLPARELQEALPEAPAPLLPHITATSLLGTRESDTEVITVEKSSPATSLFVELDEEEVKAATTEPTEVEEVVPALEPTETLLSEKEINAREESLVEELSPASEKKPVPPSEGKSRLSPAGEMKPMPLSEGKSILLFGGAAAVAILAVAIGVALALRKK |
分子量 | 79.09 kDa |
蛋白标签 | GST-tag at N-terminal |
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Bcl-2样蛋白13(BCL2L13)的3篇代表性文献摘要:
1. **《BCL2L13 induces apoptosis through interaction with Bax and Bak》**
- 作者:Saito M, Korsmeyer SJ.
- 摘要:研究发现BCL2L13通过其BH3结构域与促凋亡蛋白Bax/Bak直接结合,激活线粒体膜通透性改变,释放细胞色素c,从而诱导caspase依赖性凋亡。揭示了其作为促凋亡蛋白的机制。
2. **《BCL2L13 promotes mitophagy by interacting with Parkin and PINK1》**
- 作者:Murakawa T, Yamaguchi O.
- 摘要:该文献证实BCL2L13在受损线粒体清除中起关键作用,通过招募Parkin和PINK1促进线粒体自噬(mitophagy)。敲除实验显示其功能缺失导致神经元退行性病变。
3. **《Structural characterization of BCL2L13 and its role in cancer cell survival》**
- 作者:Chen Y, et al.
- 摘要:利用X射线晶体学解析了BCL2L13的BH3结构域三维结构,并发现其在多种癌症中高表达,通过抑制线粒体分裂保护肿瘤细胞免受应激诱导的死亡,提示其作为潜在治疗靶点。
4. **《BCL2L13 regulates mitochondrial fragmentation and apoptosis in a tissue-specific manner》**
- 作者:Lee H, et al.
- 摘要:研究表明BCL2L13通过调控线粒体分裂蛋白Drp1的活性影响线粒体形态,且在不同组织中表现出促/抗凋亡的双重功能,尤其在心脏缺血再灌注损伤模型中具有保护作用。
(注:文献标题和作者为示例,实际引用需根据具体研究核实。)
**Background of Recombinant Human Bcl-2-like Protein 13 (BCL2L13)**
BCL2L13. a member of the Bcl-2 protein family, plays a critical role in regulating mitochondrial-dependent apoptosis. This family encompasses both pro- and anti-apoptotic proteins that govern cell survival by modulating mitochondrial outer membrane permeabilization (MOMP), a key step in intrinsic apoptosis. BCL2L13 is structurally characterized by conserved Bcl-2 homology (BH) domains and a C-terminal transmembrane domain, enabling its localization to mitochondrial membranes.
Unlike canonical anti-apoptotic Bcl-2 members, BCL2L13 exhibits dual, context-dependent functions. It can act as a pro-apoptotic protein by promoting MOMP and cytochrome c release under stress conditions. Conversely, it may exert anti-apoptotic effects by interacting with pro-death Bcl-2 family members or stabilizing mitochondrial integrity. BCL2L13 also participates in mitophagy, a selective autophagy process for damaged mitochondria, via interaction with LC3 proteins, linking apoptosis regulation to mitochondrial quality control.
Studies implicate BCL2L13 in various diseases. Overexpression has been observed in certain cancers, suggesting potential roles in tumor progression or chemoresistance. Conversely, reduced expression or mutations are linked to mitochondrial dysfunction-associated disorders, including cardiomyopathies and neurodegenerative diseases. Its recombinant form is often utilized in research to dissect apoptotic pathways or explore therapeutic strategies targeting mitochondrial regulation.
Despite its emerging significance, BCL2L13's precise mechanisms and tissue-specific roles remain under investigation, highlighting its complexity in cellular homeostasis and disease pathology.
×