| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TMEM30A |
| Uniprot No | Q9NV96 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-361 aa |
| 活性数据 | MAMNYNAKDEVDGGPPCAPGGTAKTRRPDNTAFKQQRLPAWQPILTAGTVLPIFFIIGLIFIPIGIGIFVTSNNIREIEIDYTGTEPSSPCNKCLSPDVTPCFCTINFTLEKSFEGNVFMYYGLSNFYQNHRRYVKSRDDSQLNGDSSALLNPSKECEPYRRNEDKPIAPCGAIANSMFNDTLELFLIGNDSYPIPIALKKKGIAWWTDKNVKFRNPPGGDNLEERFKGTTKPVNWLKPVYMLDSDPDNNGFINEDFIVWMRTAALPTFRKLYRLIERKSDLHPTLPAGRYSLNVTYNYPVHYFDGRKRMILSTISWMGGKNPFLGIAYIAVGSISFLLGVVLLVINHKYRNSSNTADITI |
| 分子量 | 67.1 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 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. |
以下为模拟生成的关于重组人TMEM30A蛋白的参考文献示例(非真实文献，仅供格式参考)：
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1. **文献名称**: "TMEM30A regulates lipid bilayer composition in P4-ATPase-mediated vesicle transport"
**作者**: Zhang L, et al.
**摘要**: 研究证实TMEM30A作为P4-ATP酶的必需辅助因子，通过重组蛋白实验揭示其在哺乳动物细胞囊泡运输中通过调控磷脂不对称分布维持膜稳定性，缺失会导致神经细胞发育缺陷。
2. **文献名称**: "Structural insights into human TMEM30A-ATP8B1 complex by cryo-EM"
**作者**: Chen X, et al.
**摘要**: 利用冷冻电镜解析重组人TMEM30A与ATP8B1的复合体结构，阐明两者协同转运磷脂酰丝氨酸的分子机制，为胆汁淤积症相关突变提供结构基础。
3. **文献名称**: "TMEM30A deficiency drives B cell lymphoma via impaired surface receptor internalization"
**作者**: Kim S, et al.
**摘要**: 通过基因敲除模型发现，TMEM30A缺失导致B细胞受体(BCR)内吞障碍，引发持续AKT信号通路激活，促进淋巴瘤发生，提示其肿瘤抑制潜力。
4. **文献名称**: "High-yield recombinant TMEM30A production in insect cells for functional ATPase assays"
**作者**: Gonzalez R, et al.
**摘要**: 开发杆状病毒-昆虫细胞系统高效表达重组人TMEM30A蛋白，优化纯化步骤并验证其与ATP8A1的体外结合活性，推动P4-ATP酶功能研究方法标准化。
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**备注**：以上内容为虚构示例，实际文献需通过PubMed、Google Scholar等平台以**"TMEM30A"、"CDC50A"、"P4-ATPase"**等关键词检索，并结合研究领域(如膜蛋白折叠、疾病机制或重组表达技术)筛选。
TMEM30A, also known as CDC50A, is a conserved transmembrane protein critical for maintaining cell membrane asymmetry by facilitating phospholipid translocation. It serves as a β-subunit for P4-ATPases (lipid flippases), forming heterocomplexes essential for transporting phospholipids like phosphatidylserine from the outer to the inner leaflet of cellular membranes. This activity underpins vital processes including vesicle trafficking, cell signaling, and membrane repair. TMEM30A is ubiquitously expressed, with high levels in tissues like the liver, brain, and kidneys, reflecting its broad physiological relevance.
Mutations in TMEM30A are linked to human diseases. Biallelic loss-of-function variants cause autosomal recessive intrahepatic cholestasis, characterized by impaired bile flow and liver dysfunction, likely due to disrupted membrane integrity in hepatocytes. Additionally, studies associate TMEM30A dysregulation with neurological disorders and cancer progression, where its overexpression may promote tumor cell survival and metastasis. Structurally, the protein contains two transmembrane domains and a large extracellular loop, though its precise interaction mechanisms with P4-ATPases remain under investigation.
Recombinant human TMEM30A protein, produced via heterologous expression systems, enables in vitro studies of lipid transport machinery, drug screening for cholestasis, and exploration of therapeutic strategies targeting membrane-related pathologies. Its role in ATP11B/CDC50A complexes is particularly scrutinized for connections to apoptosis and neurodegenerative disease mechanisms.
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