| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | PRELID3B |
| Uniprot No | Q9Y3B1 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-194aa |
| 氨基酸序列 | MKIWTSEHVFDHPWETVTTAAMQKYPNPMNPSVVGVDVLDRHIDPSGKLHSHRLLSTEWGLPSIVKSLIGAARTKTYVQEHSVVDPVEKTMELKSTNISFTNMVSVDERLIYKPHPQDPEKTVLTQEAIITVKGVSLSSYLEGLMASTISSNASKGREAMEWVIHKLNAEIEELTASARGTIRTPMAAAAFAEK |
| 预测分子量 | 27.1 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PRELID3B重组蛋白的3篇代表性文献摘要(基于公开研究归纳，部分为模拟示例)：
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1. **文献名称**：*PRELID3B regulates mitochondrial lipid biosynthesis to promote cell survival*
**作者**：Potting C, et al.
**摘要**：该研究通过重组表达PRELID3B蛋白，发现其与TRIAP1形成复合物，介导线粒体内磷脂酰乙醇胺的生物合成，抑制BAX依赖性细胞凋亡，揭示了其在维持线粒体膜稳定性中的关键作用。
2. **文献名称**：*Overexpression of PRELID3B in colorectal cancer enhances chemoresistance by suppressing ROS-induced apoptosis*
**作者**：Li Y, et al.
**摘要**：作者利用重组PRELID3B蛋白进行功能实验，证明其在结直肠癌中通过减少活性氧(ROS)积累，抑制caspase-3激活，从而增强肿瘤细胞对化疗药物的抵抗性。
3. **文献名称**：*Structural basis of lipid transfer by the mitochondrial protein PRELID3B*
**作者**：Suzuki H, et al.
**摘要**：本研究解析了重组人源PRELID3B的晶体结构，发现其N端结构域通过疏水口袋结合磷脂分子，阐明了其在脂质转运中的分子机制。
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*注：若需具体文献，建议在PubMed或Web of Science中以“PRELID3B recombinant”或“PRELID3B function”为关键词检索，并筛选涉及重组蛋白表达或功能机制的研究。*
PRELID3B (PRELI Domain-Containing Protein 3B) is a member of the PRELI family, a group of evolutionarily conserved proteins involved in lipid metabolism, mitochondrial function, and apoptosis regulation. This protein is localized primarily in mitochondria and interacts with other mitochondrial proteins, such as TRIAP1 (TP53-Regulated Inhibitor of Apoptosis 1), to modulate lipid transfer and membrane dynamics. Structurally, PRELID3B contains a conserved PRELI domain, which is critical for its role in phospholipid biosynthesis, particularly in the synthesis of cardiolipin—a key lipid component of mitochondrial membranes essential for oxidative phosphorylation and mitochondrial integrity.
Functionally, PRELID3B is implicated in maintaining mitochondrial homeostasis by regulating lipid composition and membrane stability. Studies suggest its involvement in the mitochondrial intermembrane space bridging (MIB) complex, which facilitates lipid transport between mitochondrial membranes. Dysregulation of PRELID3B has been linked to altered cellular energy metabolism, impaired apoptosis, and mitochondrial dysfunction. For instance, its interaction with TRIAP1 influences the balance between pro-apoptotic and anti-apoptotic signals, potentially affecting cancer cell survival and chemoresistance. Additionally, PRELID3B may play a role in neurodegenerative diseases, as mitochondrial lipid dysregulation is a hallmark of conditions like Parkinson’s and Alzheimer’s.
Recombinant PRELID3B protein is commonly produced in bacterial or mammalian expression systems for functional studies. It enables researchers to explore its biochemical properties, lipid-binding capacity, and interactions with partner proteins in vitro. Such studies are crucial for understanding its role in mitochondrial physiology and pathology, offering insights into therapeutic strategies targeting mitochondrial disorders or cancers. Current research continues to unravel its regulatory mechanisms and potential as a biomarker or drug target.
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