| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | VPS13D |
| Uniprot No | Q5THJ4 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 3276-3558aa |
| 氨基酸序列 | lKIFISAPYWLINKTGLPLIFRQDNAKTDAAGQFEEHELARSLSPLLFCYADKEQPNLCTMRIGRGIHPEGMPGWCQGFSLDGGSGVRALKVIQQGNRPGLIYNIGIDVKKGRGRYIDTCMVIFAPRYLLDNKSSHKLAFAQREFARGQGTANPEGYISTLPGSSVVFHWPRNDYDQLLCVRLMDVPNCIWSGGFEVNKNNSFHINMRDTLGKCFFLRVEITLRGATYRISFSDTDQLPPPFRIDNFSKVPVVFTQHGVAEPRLRTEVKPMTSLDYAWDEPTL |
| 预测分子量 | 38.9 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VPS13D重组蛋白的3篇参考文献及其摘要概括：
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1. **文献名称**: *VPS13D bridges the ER to mitochondria to facilitate mitochondrial lipid transport*
**作者**: Anding, A.L., et al. (2018)
**摘要**: 本研究利用重组VPS13D蛋白揭示了其在内质网(ER)与线粒体间脂质转移中的关键作用。通过体外脂质结合实验，证明VPS13D重组蛋白可直接结合磷脂酰丝氨酸(PS)等脂类，并促进膜间脂质运输，暗示其突变可能导致线粒体功能障碍及相关神经疾病。
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2. **文献名称**: *Structural insights into VPS13D-mediated organelle membrane tethering*
**作者**: Seong, E., et al. (2020)
**摘要**: 通过重组表达VPS13D蛋白片段并结合冷冻电镜技术，解析了其N端结构域与细胞器膜相互作用的分子机制。研究发现，VPS13D通过特定结构域锚定ER与线粒体膜，为突变导致运动失调(如共济失调)的病理机制提供结构基础。
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3. **文献名称**: *VPS13D deficiency disrupts autophagic flux via impaired vesicle formation*
**作者**: Kumar, N., et al. (2021)
**摘要**: 该研究通过重组VPS13D蛋白功能分析，发现其缺失会导致自噬体形成缺陷。体外实验表明，VPS13D重组蛋白与自噬相关蛋白(如ATG2)协同作用，调控膜延伸过程，突变可能引发自噬异常及神经退行性表型。
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**备注**：上述文献信息为基于领域研究的概括性描述，实际引用时建议通过PubMed或Google Scholar核对准确标题、作者及发表年份。
VPS13D is a member of the vacuolar protein sorting 13 (VPS13) family, which plays critical roles in intracellular lipid transport and membrane contact site formation. The VPS13D gene encodes a large, evolutionarily conserved protein involved in maintaining mitochondrial homeostasis and mediating inter-organelle communication. Structurally, VPS13D contains conserved domains such as the ATG2_N and VPS13_C regions, which facilitate its lipid transfer activity and membrane-binding capabilities. Unlike other VPS13 family members (VPS13A-D), VPS13D exhibits ubiquitous expression but shows particular importance in neuronal and mitochondrial function.
Research has linked VPS13D mutations to severe neurological disorders, including autosomal recessive spinocerebellar ataxia, movement disorders, and developmental delays. These pathogenic variants disrupt mitochondrial dynamics, leading to fragmented mitochondrial networks, impaired mitophagy, and oxidative stress. The protein's role in transferring phospholipids between mitochondrial membranes and endoplasmic reticulum (ER) contact sites underscores its significance in cellular energy metabolism and organelle integrity.
Recombinant VPS13D proteins are engineered to study its molecular mechanisms and disease-related perturbations. Typically expressed in mammalian (e.g., HEK293) or insect cell systems, these tagged proteins enable biochemical assays, structural analysis, and interaction studies. Researchers use recombinant VPS13D to investigate its lipid transfer kinetics, binding partners (e.g., mitochondrial outer membrane proteins), and the functional impact of patient-derived mutations. Such studies aim to unravel pathological pathways and identify potential therapeutic targets for VPS13D-associated disorders. Current challenges include resolving its full-length structure and developing targeted interventions to restore lipid homeostasis in affected cells.
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