| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TRMT10C |
| Uniprot No | Q7L0Y3 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 40-403aa |
| 氨基酸序列 | MSSKIPAVTYPKNESTPPSEELELDKWKTTMKSSVQEECVSTISSSKDEDPLAATREFIEMWRLLGREVPEHITEEELKTLMECVSNTAKKKYLKYLYTKEKVKKARQIKKEMKAAAREEAKNIKLLETTEEDKQKNFLFLRLWDRNMDIAMGWKGAQAMQFGQPLVFDMAYENYMKRKELQNTVSQLLESEGWNRRNVDPFHIYFCNLKIDGALHRELVKRYQEKWDKLLLTSTEKSHVDLFPKDSIIYLTADSPNVMTTFRHDKVYVIGSFVDKSMQPGTSLAKAKRLNLATECLPLDKYLQWEIGNKNLTLDQMIRILLCLKNNGNWQEALQFVPKRKHTGFLEISQHSQEFINRLKKAKT |
| 预测分子量 | 46.5 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TRMT10C重组蛋白的3篇参考文献及其摘要概括：
1. **文献名称**: *TRMT10C is a mitochondrial methyltransferase responsible for m1G9 modification of human mitochondrial tRNAs*
**作者**: Powell CA et al.
**摘要**: 本研究解析了TRMT10C作为线粒体tRNA m1G9位点甲基转移酶的功能。通过重组蛋白表达和体外酶活实验，证实TRMT10C与ACAT1形成复合体，协同催化线粒体tRNA的甲基化修饰，并揭示其缺陷导致线粒体翻译障碍。
2. **文献名称**: *Structural insights into the molecular mechanism of the m1G methyltransferase TRMT10C*
**作者**: Suzuki T et al.
**摘要**: 利用X射线晶体学解析了重组人源TRMT10C蛋白的晶体结构，揭示了其底物结合口袋和催化关键残基。功能实验表明，TRMT10C的SAM结合域突变会显著降低其甲基转移酶活性。
3. **文献名称**: *A homozygous TRMT10C mutation causes a mitochondrial disorder associated with impaired RNA modification*
**作者**: Vilardo E et al.
**摘要**: 通过重组TRMT10C蛋白的功能研究，发现其突变体(如R323H)丧失与tRNA的结合能力，导致患者细胞中线粒体tRNA m1G9修饰缺失，进而引发线粒体脑肌病。研究强调了TRMT10C在维持线粒体功能中的必要性。
(注：部分文献为虚构示例，实际研究中建议通过PubMed等数据库以关键词“TRMT10C recombinant”或“TRMT10C methylation”检索最新成果。)
TRMT10C is a mitochondrial methyltransferase enzyme that plays a critical role in RNA modification and mitochondrial function. As a member of the TRM10 family, it catalyzes the transfer of methyl groups to specific nucleotides in mitochondrial transfer RNAs (tRNAs), particularly at the N1 position of adenine (m¹A) in tRNA transcripts. This post-transcriptional modification is essential for ensuring tRNA stability, proper folding, and accurate decoding during mitochondrial protein synthesis. TRMT10C operates in a complex with another protein, SDR5C1 (HSD10), forming a functional unit that couples tRNA methylation with NAD⁺-dependent metabolic regulation.
The gene encoding TRMT10C is located on human chromosome 3 and is ubiquitously expressed, reflecting its fundamental role in cellular energy production. Mutations in TRMT10C have been linked to mitochondrial disorders, including combined oxidative phosphorylation deficiency (COXPD) and early-onset encephalopathy, highlighting its importance in maintaining mitochondrial health. These genetic defects disrupt tRNA modification, leading to impaired mitochondrial translation, reduced respiratory chain activity, and compromised ATP synthesis.
Recombinant TRMT10C protein is engineered for in vitro studies to investigate its enzymatic mechanisms, substrate specificity, and interaction partners. Produced using bacterial or mammalian expression systems, the purified protein retains methyltransferase activity and enables biochemical characterization of its catalytic domain. Researchers employ it to explore disease-associated mutations, screen potential therapeutic compounds, and dissect the interplay between RNA modification and mitochondrial dysfunction. Its recombinant form also serves as a tool for structural studies using X-ray crystallography or cryo-EM, advancing our understanding of tRNA-modifying enzymes in mitochondrial biology and disease pathology.
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