| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | DUSP10 |
| Uniprot No | Q9Y6W6 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-140aa |
| 氨基酸序列 | MQRLNIGYVINVTTHLPLYHYEKGLFNYKRLPATDSNKQNLRQYFEEAFE FIEEAHQCGKGLLIHCQAGVSRSATIVIAYLMKHTRMTMTDAYKFVKGKR PIISPNLNFMGQLLEFEEDLNNGVTPRILTPKLMGVETVV |
| 预测分子量 | 41 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DUSP10重组蛋白的3篇参考文献示例(注：文献为假设性示例，建议通过学术数据库核实具体研究)：
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1. **标题**: *"Recombinant DUSP10 Protein Attenuates LPS-Induced Inflammation by Suppressing MAPK Signaling in Macrophages"*
**作者**: Li Y, Chen J, Wang H.
**摘要**: 本研究通过大肠杆菌系统表达并纯化了重组DUSP10蛋白，发现其通过特异性去磷酸化JNK和p38 MAPK通路，显著抑制脂多糖(LPS)诱导的巨噬细胞炎症因子释放，提示DUSP10重组蛋白在抗炎治疗中的潜在应用。
2. **标题**: *"Structural and Functional Characterization of Human DUSP10 Catalytic Domain"*
**作者**: Kumar S, et al.
**摘要**: 作者利用昆虫细胞表达系统制备了重组人源DUSP10催化结构域，并通过晶体结构解析和体外酶活实验，揭示了其底物结合的关键氨基酸残基，为设计靶向DUSP10的小分子抑制剂提供了结构基础。
3. **标题**: *"DUSP10 Recombinant Protein Enhances Cardiac Ischemia-Reperfusion Injury Recovery via ERK Pathway Modulation"*
**作者**: Zhang R, et al.
**摘要**: 实验表明，重组DUSP10蛋白通过抑制心肌细胞中ERK的过度激活，减少氧化应激和细胞凋亡，显著改善小鼠心脏缺血再灌注损伤后的功能恢复，提示其作为心脏保护剂的潜力。
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**建议**：可通过PubMed或Google Scholar搜索关键词“DUSP10 recombinant protein”或“DUSP10 expression and purification”获取真实文献。
DUSP10 (Dual Specificity Phosphatase 10), also known as MAP Kinase Phosphatase-5 (MKP-5), is a member of the dual-specificity phosphatase family. These enzymes regulate mitogen-activated protein kinase (MAPK) signaling pathways by dephosphorylating both phosphotyrosine and phosphoserine/phosphothreonine residues on MAPKs. DUSP10 specifically inactivates stress-activated MAPKs, such as p38 and JNK (c-Jun N-terminal kinase), which are critical for cellular responses to inflammation, stress, and apoptosis. Its expression is induced by various stimuli, including cytokines, oxidative stress, and Toll-like receptor (TLR) activation, highlighting its role in immune and inflammatory regulation.
Structurally, DUSP10 contains an N-terminal MAPK-binding domain (MKB) that facilitates substrate interaction and a C-terminal catalytic domain responsible for phosphatase activity. Recombinant DUSP10 protein is typically produced in bacterial or mammalian expression systems, enabling studies on its enzymatic activity, substrate specificity, and regulatory mechanisms. Researchers utilize this recombinant protein to explore its therapeutic potential in diseases linked to dysregulated MAPK signaling, such as autoimmune disorders, neurodegenerative conditions, and cancer. For example, DUSP10 overexpression has been shown to suppress excessive inflammation in models of sepsis or arthritis by dampening p38/JNK-driven cytokine production.
Despite its protective roles, DUSP10's context-dependent functions remain under investigation. In cancer, it may act as a tumor suppressor or promoter depending on the cellular environment. Recombinant DUSP10 tools are thus vital for dissecting these complexities and developing targeted therapies. Challenges include optimizing its stability, delivery, and specificity in vivo. Overall, DUSP10 recombinant protein serves as a key reagent for advancing our understanding of MAPK signaling networks and their implications in health and disease.
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