| 纯度 | >90%SDS-PAGE. |
| 种属 | mouse |
| 靶点 | Pld3 |
| Uniprot No | O35405 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-488aa |
| 氨基酸序列 | MKPKLMYQEL KVPVEEPAGE LPLNEIEAWK AAEKKARWVL LVLILAVVGF GALMTQLFLW EYGDLHLFGP NQRPAPCYDP CEAVLVESIP EGLEFPNATT SNPSTSQAWL GLLAGAHSSL DIASFYWTLT NNDTHTQEPS AQQGEEVLQQ LQALAPRGVK VRIAVSKPNG PLADLQSLLQ SGAQVRMVDM QKLTHGVLHT KFWVVDQTHF YLGSANMDWR SLTQVKELGV VMYNCSCLAR DLTKIFEAYW FLGQAGSSIP STWPRSFDTR YNQETPMEIC LNGTPALAYL ASAPPPLCPS GRTPDLKALL NVVDSARSFI YIAVMNYLPT MEFSHPRRFW PAIDDGLRRA AYERGVKVRL LISCWGHSDP SMRSFLLSLA ALHDNHTHSD IQVKLFVVPT DESQARIPYA RVNHNKYMVT ERASYIGTSN WSGSYFTETA GTSLLVTQNG HGGLRSQLEA VFLRDWESPY SHDLDTSANS VGNACRLL |
| 预测分子量 | 58 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PLD3重组蛋白研究的**示例参考文献**(仅供参考，具体文献需根据实际研究查询)：
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1. **文献名称**：*"PLD3 gene variants in Alzheimer's disease"*
**作者**：Cruchaga C. et al.
**摘要**：该研究通过遗传学分析发现PLD3基因的罕见变异与晚发性阿尔茨海默病风险显著相关，并推测PLD3可能通过调控淀粉样前体蛋白(APP)的加工影响疾病进程。文中提及利用重组PLD3蛋白验证其与APP的相互作用。
2. **文献名称**：*"Functional characterization of phospholipase D3 (PLD3) in lysosomal protein degradation"*
**作者**：Nakamura Y. et al.
**摘要**：研究通过重组PLD3蛋白体外实验，发现其具有磷脂酶活性，并参与溶酶体功能调控，可能通过水解特定磷脂分子影响自噬相关信号通路。
3. **文献名称**：*"Expression and purification of human PLD3 in a mammalian system for structural studies"*
**作者**：Lee S. et al.
**摘要**：本文报道了在HEK293细胞中高效表达重组人源PLD3蛋白的方法，通过亲和层析纯化获得高纯度蛋白，并解析了其部分结构特征，为后续功能研究奠定基础。
4. **文献名称**：*"PLD3 modulates EGFR signaling in cancer cell invasion"*
**作者**：Smith J. et al.
**摘要**：研究利用重组PLD3蛋白进行细胞实验，发现其通过调控表皮生长因子受体(EGFR)的磷酸化状态，抑制肿瘤细胞的迁移和侵袭能力。
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**注意**：以上为示例性内容，实际文献需通过数据库(如PubMed、Web of Science)检索确认。PLD3研究多集中于神经退行性疾病和癌症领域，重组蛋白相关文献可能涉及表达方法、酶学特性或功能机制分析。
**Background of PLD3 Recombinant Protein**
Phospholipase D3 (PLD3) is a member of the phospholipase D superfamily, which plays roles in lipid metabolism, membrane trafficking, and intracellular signaling. Unlike its well-studied paralogs PLD1 and PLD2. PLD3 lacks the canonical HxKxxxxD (HKD) catalytic motifs typical of phospholipases, suggesting distinct functional mechanisms. Initially identified as a susceptibility gene in late-onset Alzheimer’s disease (LOAD), PLD3 gained attention due to genetic studies linking rare coding variants to altered amyloid-beta processing. However, its precise biological role remains poorly understood.
Recombinant PLD3 protein is engineered to enable functional and structural studies. Produced via heterologous expression systems (e.g., mammalian or insect cells), it retains post-translational modifications critical for activity. Research focuses on clarifying PLD3’s enzymatic activity, with conflicting reports on its ability to hydrolyze phospholipids or other substrates. Recent studies propose non-enzymatic roles, such as modulating endosomal-lysosomal trafficking or interacting with neurodegenerative disease-related proteins like APP.
The development of PLD3 recombinant protein has advanced investigations into its pathophysiological relevance. In vitro assays using purified PLD3 have explored its interaction with lipid membranes and potential regulatory partners. Structural analyses, though limited, aim to resolve its unique fold and active site architecture. Challenges persist in reconciling its genetic association with Alzheimer’s disease and its molecular function, driving demand for high-quality recombinant tools.
Overall, PLD3 recombinant protein serves as a key reagent to unravel its enigmatic role in cellular homeostasis and disease, offering insights for therapeutic targeting in neurodegeneration and beyond.
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