| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | MAPK7 |
| Uniprot No | Q13164 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-816aa |
| 氨基酸序列 | MAEPLKEEDGEDGSAEPPGPVKAEPAHTAASVAAKNLALLKARSFDVTFDVGDEYEIIETIGNGAYGVVSSARRRLTGQQVAIKKIPNAFDVVTNAKRTLRELKILKHFKHDNIIAIKDILRPTVPYGEFKSVYVVLDLMESDLHQIIHSSQPLTLEHVRYFLYQLLRGLKYMHSAQVIHRDLKPSNLLVNENCELKIGDFGMARGLCTSPAEHQYFMTEYVATRWYRAPELMLSLHEYTQAIDLWSVGCIFGEMLARRQLFPGKNYVHQLQLIMMVLGTPSPAVIQAVGAERVRAYIQSLPPRQPVPWETVYPGADRQALSLLGRMLRFEPSARISAAAALRHPFLAKYHDPDDEPDCAPPFDFAFDREALTRERIKEAIVAEIEDFHARREGIRQQIRFQPSLQPVASEPGCPDVEMPSPWAPSGDCAMESPPPAPPPCPGPAPDTIDLTLQPPPPVSEPAPPKKDGAISDNTKAALKAALLKSLRSRLRDGPSAPLEAPEPRKPVTAQERQREREEKRRRRQERAKEREKRRQERERKERGAGASGGPSTDPLAGLVLSDNDRSLLERWTRMARPAAPALTSVPAPAPAPTPTPTPVQPTSPPPGPVAQPTGPQPQSAGSTSGPVPQPACPPPGPAPHPTGPPGPIPVPAPPQIATSTSLLAAQSLVPPPGLPGSSTPGVLPYFPPGLPPPDAGGAPQSSMSESPDVNLVTQQLSKSQVEDPLPPVFSGTPKGSGAGYGVGFDLEEFLNQSFDMGVADGPQDGQADSASLSASLLADWLEGHGMNPADIESLQREIQMDSPMLLADLPDLQDP |
| 预测分子量 | 88,3 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MAPK7重组蛋白的3篇文献示例(内容基于公开研究总结，非真实文献)：
1. **"ERK5/MAPK7重组蛋白的制备及其在炎症信号通路中的作用"**
- 作者：Yeung, K. et al.
- 摘要：研究利用昆虫细胞系统表达并纯化重组MAPK7蛋白，揭示其通过磷酸化下游转录因子(如MEF2)调控炎症反应，并验证其激酶活性依赖MEK5的激活。
2. **"重组MAPK7在肿瘤细胞增殖中的功能分析"**
- 作者：Nakamura, K. et al.
- 摘要：通过大肠杆菌表达重组MAPK7.证明其过表达促进癌细胞增殖和侵袭，并发现其通过激活c-Jun通路增强肿瘤生长，为靶向治疗提供依据。
3. **"MAPK7重组蛋白的结构解析与药物筛选平台开发"**
- 作者：Drew, B.A. et al.
- 摘要：利用哺乳动物细胞系表达高纯度MAPK7重组蛋白，结合X射线晶体学解析其三维结构，并基于此筛选小分子抑制剂，验证其抗肿瘤潜力。
(注：以上为模拟摘要，实际文献需通过数据库如PubMed检索确认。)
**Background of MAPK7 Recombinant Protein**
Mitogen-activated protein kinase 7 (MAPK7), also known as extracellular signal-regulated kinase 5 (ERK5), is a member of the MAPK family, which plays pivotal roles in regulating cellular responses to external stimuli. Unlike other MAPKs, MAPK7 contains a unique C-terminal domain in addition to its kinase domain, enabling distinct regulatory mechanisms and substrate interactions. It is activated through dual phosphorylation by upstream MAPK kinases (MEK5) on threonine and tyrosine residues within a conserved TEY motif, triggering its translocation to the nucleus to modulate gene expression.
MAPK7 is involved in diverse physiological processes, including cell proliferation, differentiation, survival, and stress responses. It is particularly critical during embryogenesis, cardiovascular development, and neuronal function. Dysregulation of MAPK7 signaling has been implicated in pathologies such as cancer, cardiovascular diseases, and neurodegenerative disorders, highlighting its therapeutic relevance.
Recombinant MAPK7 protein is engineered for in vitro studies to dissect its biochemical activity, structural features, and interactions with substrates or inhibitors. Produced using expression systems like *E. coli* or mammalian cells, the recombinant form often retains post-translational modifications crucial for functionality when expressed in eukaryotic hosts. Researchers employ it in kinase assays, protein-protein interaction studies, and high-throughput drug screening to identify modulators of the ERK5 pathway.
The availability of MAPK7 recombinant protein has advanced the development of targeted therapies, particularly in oncology, where aberrant ERK5 signaling promotes tumor growth and metastasis. Its study also aids in understanding cross-talk with other MAPK pathways, offering insights into cellular signaling complexity. Overall, MAPK7 recombinant tools remain indispensable for both basic research and translational applications.
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