| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ATP6V0A1 |
| Uniprot No | Q93050 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-831aa |
| 氨基酸序列 | MGELFRSEEMTLAQLFLQSEAAYCCVSELGELGKVQFRDLNPDVNVFQRKFVNEVRRCEEMDRKLRFVEKEIRKANIPIMDTGENPEVPFPRDMIDLEANFEKIENELKEINTNQEALKRNFLELTELKFILRKTQQFFDEMADPDLLEESSSLLEPSEMGRGTPLRLGFVAGVINRERIPTFERMLWRVCRGNVFLRQAEIENPLEDPVTGDYVHKSVFIIFFQGDQLKNRVKKICEGFRASLYPCPETPQERKEMASGVNTRIDDLQMVLNQTEDHRQRVLQAAAKNIRVWFIKVRKMKAIYHTLNLCNIDVTQKCLIAEVWCPVTDLDSIQFALRRGTEHSGSTVPSILNRMQTNQTPPTYNKTNKFTYGFQNIVDAYGIGTYREINPAPYTIITFPFLFAVMFGDFGHGILMTLFAVWMVLRESRILSQKNENEMFSTVFSGRYIILLMGVFSMYTGLIYNDCFSKSLNIFGSSWSVRPMFTYNWTEETLRGNPVLQLNPALPGVFGGPYPFGIDPIWNIATNKLTFLNSFKMKMSVILGIIHMLFGVSLSLFNHIYFKKPLNIYFGFIPEIIFMTSLFGYLVILIFYKWTAYDAHTSENAPSLLIHFINMFLFSYPESGYSMLYSGQKGIQCFLVVVALLCVPWMLLFKPLVLRRQYLRRKHLGTLNFGGIRVGNGPTEEDAEIIQHDQLSTHSEDADEFDFGDTMVHQAIHTIEYCLGCISNTASYLRLWALSLAHAQLSEVLWTMVIHIGLSVKSLAGGLVLFFFFTAFATLTVAILLIMEGLSAFLHALRLHWVEFQNKFYSGTGFKFLPFSFEHIREGKFEE |
| 分子量 | 122.2 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ATP6V0A1(V-ATP酶V0a1亚基)研究的示例文献摘要(仅供参考，实际文献需通过数据库验证)：
---
1. **文献名称**：*Structural insights into human V-ATPase subunit ATP6V0A1 assembly and function*
**作者**：Smith A, et al.
**摘要**：研究解析了重组人ATP6V0A1蛋白的晶体结构，揭示了其在V-ATP酶复合体组装中的关键作用，并发现其C端结构域介导质子转运功能。
2. **文献名称**：*Recombinant ATP6V0A1 expression in HEK293 cells: Implications for lysosomal acidification defects*
**作者**：Zhang Y, et al.
**摘要**：通过哺乳动物系统表达重组ATP6V0A1.证明该蛋白功能缺陷可导致溶酶体酸化异常，与神经退行性疾病相关。
3. **文献名称**：*ATP6V0A1 mutations disrupt autophagy via impaired V-ATPase activity*
**作者**：Wang L, et al.
**摘要**：利用重组蛋白模型，揭示了ATP6V0A1基因突变通过损害V-ATP酶活性影响自噬小体酸化，进而导致代谢疾病的分子机制。
4. **文献名称**：*Targeting ATP6V0A1 in cancer: Recombinant protein-based drug screening*
**作者**：Kim H, et al.
**摘要**：通过原核系统表达功能性重组ATP6V0A1.开发针对该亚基的小分子抑制剂，证明其可抑制肿瘤细胞外微环境酸化。
---
**说明**：上述文献为简化示例，实际引用需在PubMed、Google Scholar等平台搜索以下关键词：
`recombinant human ATP6V0A1`、`V-ATPase V0a1 subunit`、`proton pump assembly`、`lysosomal acidification`。
The vacuolar-type H⁺-ATPase (V-ATPase) is a multisubunit proton pump critical for acidifying intracellular compartments (e.g., lysosomes, endosomes) and regulating extracellular pH in specialized cells. The V-ATP6V0A1 protein, also known as subunit a1 of the V-ATPase V0 domain, is a key isoform of the transmembrane sector responsible for proton translocation. It is encoded by the ATP6V0A1 gene and plays distinct roles in organelle-specific acidification, membrane trafficking, and cell signaling. Subunit a1 is predominantly expressed in kidney, osteoclasts, and neurons, where its activity supports processes like urinary acidification, bone resorption, and synaptic vesicle recycling. Dysregulation of V-ATP6V0A1 is linked to diseases such as renal tubular acidosis, osteoporosis, and neurodegenerative disorders. Its overexpression in certain cancers has been associated with tumor metastasis via microenvironment acidification. Recombinant human V-ATP6V0A1 protein is produced in heterologous systems (e.g., mammalian or insect cells) for structural and functional studies, enabling exploration of its role in pH homeostasis and disease mechanisms. Research on this protein aids in developing targeted therapies, including V-ATPase inhibitors for cancer or osteoclast-modulating drugs for bone diseases. Structural insights into its interaction with other V0 subunits may reveal mechanisms of proton channel regulation.
×
