| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | GFM2 |
| Uniprot No | Q969S9 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-779aa |
| 氨基酸序列 | MLTNLRIFAMSHQTIPSVYINNICCYKIRASLKRLKPHVPLGRNCSSLPGLIGNDIKSLHSIINPPIAKIRNIGIMAHIDAGKTTTTERILYYSGYTRSLGDVDDGDTVTDFMAQERERGITIQSAAVTFDWKGYRVNLIDTPGHVDFTLEVERCLRVLDGAVAVFDASAGVEAQTLTVWRQADKHNIPRICFLNKMDKTGASFKYAVESIREKLKAKPLLLQLPIGEAKTFKGVVDVVMKEKLLWNCNSNDGKDFERKPLLEMNDPELLKETTEARNALIEQVADLDDEFADLVLEEFSENFDLLPAEKLQTAIHRVTLAQTAVPVLCGSALKNKGIQPLLDAVTMYLPSPEERNYEFLQWYKDDLCALAFKVLHDKQRGPLVFMRIYSGTIKPQLAIHNINGNCTERISRLLLPFADQHVEIPSLTAGNIALTVGLKHTATGDTIVSSKSSALAAARRAEREGEKKHRQNNEAERLLLAGVEIPEPVFFCTIEPPSLSKQPDLEHALKCLQREDPSLKVRLDPDSGQTVLCGMGELHIEIIHDRIKREYGLETYLGPLQVAYRETILNSVRATDTLDRTLGDKRHLVTVEVEARPIETSSVMPVIEFEYAESINEGLLKVSQEAIENGIHSACLQGPLLGSPIQDVAITLHSLTIHPGTSTTMISACVSRCVQKALKKADKQVLEPLMNLEVTVARDYLSPVLADLAQRRGNIQEIQTRQDNKVVIGFVPLAEIMGYSTVLRTLTSGSATFALELSTYQAMNPQDQNTLLNRRSGLT |
| 预测分子量 | 86,6 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. |
以下是基于学术文献模式的模拟参考文献示例(请注意，这些为假设性示例，实际文献需通过学术数据库查询)：
1. **《Recombinant GFM2 expression in E. coli and its role in mitochondrial translation》**
- 作者：Chen L, et al.
- 摘要：本研究通过原核表达系统成功制备重组GFM2蛋白，验证其作为线粒体翻译延伸因子的GTP酶活性，并证明其缺陷导致HeLa细胞线粒体蛋白合成异常。
2. **《Structural analysis of human GFM2 reveals mechanisms of ribosome recycling》**
- 作者：Smith J, et al.
- 摘要：通过X射线晶体学解析重组GFM2蛋白的三维结构，揭示其与线粒体核糖体结合的分子机制，为遗传性线粒体疾病的突变位点提供结构依据。
3. **《GFM2 mutations and Parkinson's disease: Functional rescue by recombinant protein delivery》**
- 作者：Wang Y, et al.
- 摘要：在帕金森病细胞模型中，重组GFM2蛋白的递送修复了线粒体翻译功能缺陷，表明其作为潜在治疗靶点的价值。
4. **《High-yield production of bioactive GFM2 in Pichia pastoris for drug screening》**
- 作者：Kim S, et al.
- 摘要：利用毕赤酵母系统高效表达具有生物活性的重组GFM2蛋白，并建立基于该蛋白的线粒体疾病药物筛选平台。
**建议**：实际文献可通过PubMed或Web of Science搜索关键词“GFM2 recombinant”、“GFM2 mitochondrial”、“GUF2 protein”获取，重点关注近五年《Nature Cell Biology》《Cell Metabolism》等期刊。
GFM2 (GTP-dependent ribosome recycling factor mitochondrial 2), also known as mtRF2. is a mitochondrial protein critical for translation termination and ribosome recycling in mitochondrial protein synthesis. It belongs to the ribosome recycling factor (RRF) family and operates in coordination with mitochondrial release factors (mtRFs) to dissociate ribosomes after the completion of protein synthesis. GFM2 is essential for maintaining mitochondrial function, as it ensures efficient recycling of ribosomes for subsequent rounds of translation, supporting energy production via oxidative phosphorylation.
Research has shown that GFM2 mutations are linked to mitochondrial disorders, including combined oxidative phosphorylation deficiencies and neurological impairments. These findings highlight its role in mitochondrial health and cellular metabolism. Recombinant GFM2 protein is produced using biotechnological platforms (e.g., E. coli or mammalian expression systems) to study its molecular interactions, structural properties, and functional mechanisms. Purification typically involves affinity chromatography, yielding high-purity protein for biochemical assays, structural studies (e.g., cryo-EM), or drug screening.
Interest in recombinant GFM2 stems from its potential as a therapeutic target for mitochondrial diseases and conditions involving energy dysregulation, such as neurodegenerative disorders and cancer. Additionally, it serves as a tool to decipher mitochondrial translation regulation, offering insights into evolutionary conservation of ribosome recycling pathways across species. Ongoing studies aim to elucidate its interplay with other mitochondrial factors and explore strategies to modulate its activity for clinical applications.
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