| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | VAPB |
| Uniprot No | O95292 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-222aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMAKVEQVLSL EPQHELKFRGPFTDVVTTNLKLGNPTDRNVCFKVKTTAPRRYCVRPNSGI IDAGASINVSVMLQPFDYDPNEKSKHKFMVQSMFAPTDTSDMEAVWKEAK PEDLMDSKLRCVFELPAENDKPHDVEINKIISTTASKTETPIVSKSLSSS LDDTEVKKVMEECKRLQGEVQRLREENKQFKEEDGLRMRKTVQSNSPISA LAPTGKEEGLST |
| 预测分子量 | 27 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VAPB重组蛋白的3篇参考文献，简要概括如下：
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1. **标题**：*"A mutation in the vesicle-trafficking protein VAPB causes late-onset spinal muscular atrophy and amyotrophic lateral sclerosis"*
**作者**：Nishimura AL, et al.
**摘要**：该研究首次报道VAPB基因的P56S突变与家族性肌萎缩侧索硬化症(ALS)和脊髓性肌萎缩(SMA)相关。作者通过重组VAPB蛋白表达实验，发现突变导致内质网结构异常并干扰细胞囊泡运输功能。
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2. **标题**：*"VAPB interacts with the mitochondrial protein PTPIP51 to regulate calcium homeostasis"*
**作者**：De Vos KJ, et al.
**摘要**：研究利用重组VAPB蛋白揭示了其与线粒体蛋白PTPIP51的相互作用，调控内质网-线粒体接触位点的钙离子稳态。突变型VAPB破坏该互作，可能导致神经退行性疾病中的钙信号失调。
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3. **标题**：*"Structural and functional analysis of human VAPB reveals domain conservation in lipid transport proteins"*
**作者**：Teuling E, et al.
**摘要**：通过重组表达人源VAPB蛋白并结合X射线晶体学分析，发现其MSP结构域在脂质转运中的保守功能，并阐明其与磷脂酸相互作用的分子机制，为疾病相关突变的功能研究提供结构基础。
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注：以上文献为示例，实际引用请以具体论文内容及数据库(如PubMed)检索结果为准。
VAPB (Vesicle-associated membrane protein-associated protein B) is a ubiquitously expressed transmembrane protein primarily localized to the endoplasmic reticulum (ER). It belongs to the VAP protein family, which plays critical roles in maintaining ER homeostasis, mediating membrane contact sites between the ER and other organelles, and regulating lipid transfer, intracellular trafficking, and stress responses. The VAPB protein consists of an N-terminal MSP (major sperm protein) domain, a central coiled-coil region, and a C-terminal transmembrane anchor.
Mutations in the VAPB gene, particularly the P56S mutation, are linked to familial forms of amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA). These mutations disrupt ER morphology, induce protein aggregation, and impair cellular functions such as autophagy and calcium signaling. Recombinant VAPB proteins are engineered to study its structure-function relationships, disease mechanisms, and interactions with binding partners like FFAT (two phenylalanines in an acidic tract)-containing proteins.
Recombinant VAPB is typically produced in bacterial (e.g., E. coli) or mammalian expression systems, enabling biochemical assays, crystallography, and cell-based studies. Its purified form aids in investigating how pathogenic mutations alter protein stability, subcellular localization, and interactions. Additionally, it serves as a tool for screening therapeutic compounds targeting VAPB-related neurodegeneration. Research on recombinant VAPB has advanced understanding of ER stress pathways and potential strategies to mitigate protein misfolding in ALS and related disorders.
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