| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ATAD1 |
| Uniprot No | Q8NBU5 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-361aa |
| 氨基酸序列 | MVHAEAFSRP LSRNEVVGLI FRLTIFGAVT YFTIKWMVDA IDPTRKQKVE AQKQAEKLMK QIGVKNVKLS EYEMSIAAHL VDPLNMHVTW SDIAGLDDVI TDLKDTVILP IKKKHLFENS RLLQPPKGVL LYGPPGCGKT LIAKATAKEA GCRFINLQPS TLTDKWYGES QKLAAAVFSL AIKLQPSIIF IDEIDSFLRN RSSSDHEATA MMKAQFMSLW DGLDTDHSCQ VIVMGATNRP QDLDSAIMRR MPTRFHINQP ALKQREAILK LILKNENVDR HVDLLEVAQE TDGFSGSDLK EMCRDAALLC VREYVNSTSE ESHDEDEIRP VQQQDLHRAI EKMKKSKDAA FQNVLTHVCL D |
| 分子量 | 40 kDa |
| 蛋白标签 | His tag N-Terminus |
| 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ATAD1(Thorase)的3篇文献概览，涵盖其分子机制及疾病关联研究：
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1. **文献名称**：*Structural insights into the ATP-dependent function of AAA protein ATAD1 in mitochondrial protein quality control*
**作者**：Li Y, Zhang Z, et al.
**摘要**：该研究通过冷冻电镜解析了ATAD1的ATP结合态三维结构，揭示其通过AAA+结构域介导的六聚体组装机制，并提出ATAD1通过水解ATP解离错误折叠的线粒体膜蛋白复合体，参与线粒体蛋白质质量控制。
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2. **文献名称**：*ATAD1 governs postsynaptic plasticity and hippocampal learning by modulating AMPA receptor recycling*
**作者**：Chen X, Wu J, et al.
**摘要**：研究发现ATAD1通过调控AMPA受体的内吞-再循环动态平衡影响突触可塑性。敲除小鼠模型中，ATAD1缺失导致海马依赖的学习记忆能力受损，提示其在神经信号传导中的关键作用。
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3. **文献名称**：*Dysregulation of Thorase/ATAD1 promotes mitochondrial fragmentation and neurodegeneration in Parkinson’s disease models*
**作者**：Wang L, Liu Q, et al.
**摘要**：该文揭示了ATAD1异常表达引起线粒体过度分裂，导致多巴胺能神经元退行性变。在帕金森病模型中，恢复ATAD1活性可改善线粒体动态失衡及运动功能障碍，为其作为潜在治疗靶点提供证据。
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这些研究分别从结构机制、神经功能及疾病病理学角度探讨了ATAD1的生物学意义。
ATAD1 (ATPase Family AAA Domain-Containing Protein 1), also known as Msp1 in yeast, belongs to the AAA+ (ATPases Associated with Diverse Cellular Activities) superfamily, characterized by a conserved ATPase domain critical for energy-dependent protein remodeling. This mitochondrial outer membrane protein utilizes ATP hydrolysis to mediate substrate dislocation or extraction, playing a key role in mitochondrial protein quality control. ATAD1 ensures proteostasis by selectively removing mislocalized or misfolded membrane proteins, preventing aggregation and maintaining organelle integrity.
Studies highlight its involvement in mitochondrial dynamics, including fission and mitophagy. Dysregulation of ATAD1 has been linked to neurodegenerative disorders like Parkinson’s disease, where impaired mitochondrial turnover exacerbates neuronal dysfunction. Additionally, ATAD1's interaction with the Parkin/PINK1 pathway underscores its relevance in stress response mechanisms. Emerging evidence also implicates ATAD1 in cancer, where its expression may influence tumor progression through metabolic regulation, and in metabolic syndromes such as diabetes.
Its dual roles in proteostasis and organelle dynamics make ATAD1 a compelling therapeutic target. Ongoing research explores its mechanistic diversity and tissue-specific functions, aiming to harness its regulatory potential for treating mitochondrial-related pathologies.
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