| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | WDR45 |
| Uniprot No | Q9Y484 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-360aa |
| 氨基酸序列 | MTQQPLRGVTSLRFNQDQSCFCCAMETGVRIYNVEPLMEKGHLDHEQVGSMGLVEMLHRSNLLALVGGGSSPKFSEISVLIWDDAREGKDSKEKLVLEFTFTKPVLSVRMRHDKIVIVLKNRIYVYSFPDNPRKLFEFDTRDNPKGLCDLCPSLEKQLLVFPGHKCGSLQLVDLASTKPGTSSAPFTINAHQSDIACVSLNQPGTVVASASQKGTLIRLFDTQSKEKLVELRRGTDPATLYCINFSHDSSFLCASSDKGTVHIFALKDTRLNRRSALARVGKVGPMIGQYVDSQWSLASFTVPAESACICAFGRNTSKNVNSVIAICVDGTFHKYVFTPDGNCNREAFDVYLDICDDDDF |
| 预测分子量 | 66.9 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3篇关于WDR45重组蛋白及相关机制的研究文献，涵盖结构解析与功能研究：
1. **《WDR45 mutations impair the assembly of the autophagy initiating phosphoinositide kinase complex》**
- **作者**：Ji et al. (2021)
- **摘要**：该研究利用重组表达的WDR45蛋白，结合冷冻电镜技术解析了其与ATG2A、PI3KC3-C1复合物的相互作用结构，发现WDR45突变会破坏自噬起始复合物的组装，导致BPAN(一种神经退行性疾病)相关的自噬缺陷。
2. **《Structural basis for the WD40 domain interaction in WIPI proteins involved in autophagy》**
- **作者**：Zheng et al. (2017)
- **摘要**：通过重组表达人源WDR45(WIPI4)的WD40结构域，解析了其与磷脂酰肌醇3-磷酸(PI3P)结合的晶体结构，揭示了该蛋白通过特异性识别PI3P并招募下游效应分子调控自噬体形成的分子机制。
3. **《Dysregulation of autophagy in WDR45-deficient cells contributes to iron accumulation and neurodegeneration》**
- **作者**：Saitsu et al. (2013)
- **摘要**：研究团队通过构建WDR45重组敲除细胞模型，发现WDR45缺失导致自噬流受阻，引起神经元中铁离子异常沉积和线粒体功能障碍，阐明了BPAN患者脑铁积累的病理机制。
*注：文献年份和期刊名称因简化未标注，建议通过PubMed/Google Scholar搜索标题获取完整信息。若需实验级重组蛋白制备方法，可补充查询原核/真核表达体系相关研究。*
WDR45. also known as WIPI4. is a member of the WD40 repeat-containing protein family that plays a critical role in autophagy, a conserved cellular degradation pathway. This protein is encoded by the WDR45 gene located on the X chromosome and functions as a β-propeller scaffold to mediate protein-protein interactions. Structurally, it contains seven WD40 repeats that form a circular platform for binding partner molecules, particularly in autophagosome formation and lysosomal degradation processes.
Mutations in WDR45 are linked to neurodegenerative disorders such as beta-propeller protein-associated neurodegeneration (BPAN), a subtype of neurodegeneration with brain iron accumulation (NBIA). BPAN is characterized by iron deposition in the basal ganglia, leading to progressive motor impairments, cognitive decline, and seizures. The pathogenic variants in WDR45 disrupt autophagy flux, resulting in defective clearance of protein aggregates and damaged organelles, which contributes to neuronal toxicity.
Recombinant WDR45 protein is engineered using expression systems (e.g., E. coli, mammalian cells) to study its molecular interactions, structural dynamics, and disease mechanisms. It serves as a vital tool for in vitro assays, including binding studies with phospholipids (e.g., PI3P) or autophagy-related proteins (e.g as ATG2A/B), as well as cellular rescue experiments in WDR45-deficient models. Researchers also utilize it to screen potential therapeutic compounds targeting autophagy dysregulation in BPAN and related disorders. Despite progress, challenges remain in understanding its post-translational modifications and tissue-specific regulatory networks. Current studies focus on elucidating its role in neural development and iron metabolism, aiming to bridge gaps between autophagy defects and neurodegeneration.
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