| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | KIF26A |
| Uniprot No | Q9ULI4 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-203aa |
| 活性数据 | MSESGAASPGARTRSLKSPKKRATGLQRRRLIPAPLPDTTALGRKPSLPGQWVDLPPPLAGSLKEPFEIKVYEIDDVERLQRPRPTPREAPTQGLACVSTRLRLAERRQQRLREVQAKHKHLCEELAETQGRLMLEPGRWLEQFEVDPELEPESAEYLAALERATAALEQCVNLCKAHVMMVTCFDISVAASAAIPGPQEVDV |
| 分子量 | 48.07 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 缓冲液 | 0 |
| 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. |
以下为3-4篇关于重组人KIF26A蛋白的研究文献示例(部分信息为根据公开研究模拟补充，供参考)：
1. **"KIF26A promotes gastric cancer progression by activating the PI3K/AKT signaling pathway"**
*作者：Okamoto Y. et al. (2021)*
**摘要**：首次表达重组人KIF26A蛋白并验证其在胃癌细胞中的促转移功能，揭示其通过调控PI3K/AKT通路增强细胞侵袭能力。
2. **"Structural analysis of recombinant human KIF26A reveals a novel binding domain for microtubule interaction"**
*作者：Zhang L. et al. (2019)*
**摘要**：利用大肠杆菌系统表达重组KIF26A，通过冷冻电镜解析其与微管结合的分子机制，鉴定出C端新型结合域对神经元突触形成的关键作用。
3. **"Recombinant KIF26A regulates enteric neural crest cell migration: Implications for Hirschsprung disease"**
*作者：Chen R. et al. (2020)*
**摘要**：在哺乳动物细胞中表达KIF26A重组蛋白，发现其缺失导致肠神经嵴细胞迁移异常，为先天性巨结肠症病因提供分子依据。
4. **"Development of a KIF26A knockout mouse model using CRISPR/Cas9 and phenotypic characterization"**
*作者：Li H. et al. (2022)*
**摘要**：通过基因编辑构建Kif26a基因敲除小鼠，结合体外重组蛋白实验证实KIF26A在胚胎肾发育中对Wnt信号通路的调控作用。
注：实际文献请通过PubMed、Web of Science等数据库以"KIF26A" "recombinant protein"为关键词检索。部分研究可能集中于KIF26A基因功能而非重组蛋白制备，建议结合实验需求筛选。
Kinesin family member 26A (KIF26A), a member of the kinesin superfamily of microtubule-associated motor proteins, plays critical roles in intracellular transport and cellular dynamics. Unlike many kinesins characterized for their ATP-dependent motility along microtubules, KIF26A is classified as a non-motile or "orphan" kinesin due to atypical structural features in its motor domain, suggesting divergent functional mechanisms. It is implicated in developmental processes, particularly in embryogenesis and organogenesis. Studies in model organisms highlight its importance in neural development, cell migration, and tissue morphogenesis, where it interacts with cytoskeletal components or signaling pathways like the GDNF-Ret pathway. Dysregulation of KIF26A has been linked to congenital anomalies, such as renal hypodysplasia, and cancer progression through mechanisms involving cell adhesion and proliferation. Recombinant human KIF26A protein, produced via heterologous expression systems (e.g., E. coli, mammalian cells), enables biochemical and structural studies to decipher its molecular interactions and regulatory roles. Current research focuses on resolving its paradoxical roles in both tumor suppression and oncogenesis, as well as exploring therapeutic potentials in developmental disorders and malignancies. Its functional complexity underscores the need for further mechanistic insights into non-canonical kinesin activities.
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