| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CHMP2B |
| Uniprot No | Q9UQN3 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-213aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMASLFKKKTVDDVIKEQNRELRGTQRAIIR DRAALEKQEKQLELEIKKMAKIGNKEACKVLAKQLVHLRKQKTRTFAVSS KVTSMSTQTKVMNSQMKMAGAMSTTAKTMQAVNKKMDPQKTLQTMQNFQK ENMKMEMTEEMINDTLDDIFDGSDDEEESQDIVNQVLDEIGIEISGKMAK APSAARSLPSASTSKATISDEEIERQLKALGVD |
| 预测分子量 | 26 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CHMP2B重组蛋白的3篇参考文献，涵盖结构、功能及疾病关联研究：
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1. **标题**：*Mutations in the endosomal ESCRTIII-complex subunit CHMP2B in frontotemporal dementia*
**作者**：Skibinski, G. et al. (2005)
**摘要**：该研究首次发现CHMP2B基因突变与家族性额颞叶痴呆(FTD)的关联，通过重组蛋白实验揭示突变导致ESCRT-III复合体功能异常，影响胞内蛋白运输和自噬溶酶体途径。
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2. **标题**：*Structural basis of CHMP2B polymerization into helical filaments on membranes*
**作者**：Zhen, Y. et al. (2020)
**摘要**：利用重组CHMP2B蛋白的体外表达与冷冻电镜技术，解析了其结合脂质膜时聚合形成螺旋纤维的结构机制，揭示了其在膜重塑过程中的动态组装特性。
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3. **标题**：*CHMP2B regulates autophagy in motor neurons and knockdown causes neuronal degeneration*
**作者**：Lee, J.A. et al. (2010)
**摘要**：通过重组CHMP2B蛋白的过表达与敲低模型，证明其在运动神经元自噬调控中的关键作用，并发现功能缺失导致异常蛋白聚集及神经退行性表型，提示与ALS的病理关联。
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*注*：以上文献年份及内容为示例，建议通过PubMed或Web of Science核对最新研究。如需具体实验方法，可补充筛选涉及重组蛋白表达/纯化的原始研究。
CHMP2B (Charged Multivesicular Body Protein 2B) is a key component of the Endosomal Sorting Complex Required for Transport (ESCRT) machinery, which regulates membrane remodeling and scission processes critical for multivesicular body formation, cytokinesis, and viral budding. As a subunit of the ESCRT-III complex, CHMP2B assembles into filamentous polymers that constrict membranes, often in coordination with the AAA+ ATPase Vps4. Its function is essential for maintaining endolysosomal trafficking, autophagy, and cellular homeostasis.
Recombinant CHMP2B protein is engineered for in vitro studies to dissect its structural and mechanistic roles in ESCRT-mediated pathways. Typically expressed in bacterial (e.g., *E. coli*) or mammalian systems, the recombinant protein retains the ability to oligomerize and bind partners like CHMP4B or Vps4. enabling reconstitution of ESCRT-III dynamics. Purification often involves affinity tags (e.g., His-tag) followed by ion-exchange or size-exclusion chromatography to isolate functional monomers or polymers.
Mutations in CHMP2B, such as the pathogenic intron 5 splice-site mutation linked to frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS), cause C-terminal truncations that impair ESCRT disassembly. Recombinant mutant variants are used to model aberrant protein aggregation, lysosomal dysfunction, and autophagy defects observed in neurodegenerative diseases. Structural studies using X-ray crystallography or cryo-EM have revealed how CHMP2B’s conserved MIT domain interacts with Vps4 and how disease mutations disrupt helical bundle formation.
Researchers also employ CHMP2B recombinant protein in drug screening assays targeting ESCRT dysregulation in cancer and neurodegeneration. Its role in HIV-1 budding further makes it a candidate for antiviral studies. By providing a controlled, post-translationally modified product, recombinant CHMP2B bridges molecular biology and disease pathology, offering insights into membrane biology and therapeutic strategies.
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