纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | MRPS35 |
Uniprot No | P82673 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 1-323 aa |
活性数据 | MAAAALPAWLSLQSRARTLRAFSTAVYSATPVPTPSLPERTPGNERPPRRKALPPRTEKMAVDQDWPSVYPVAAPFKPSAVPLPVRMGYPVKKGVPMAKEGNLELLKIPNFLHLTPVAIKKHCEALKDFCTEWPAALDSDEKCEKHFPIEIDSTDYVSSGPSVRNPRARVVVLRVKLSSLNLDDHAKKKLIKLVGERYCKTTDVLTIKTDRCPLRRQNYDYAVYLLTVLYHESWNTEEWEKSKTEADMEEYIWENSSSERNILETLLQMKAAEKNMEINKEELLGTKEIEEYKKSVVSLKNEEENENSISQYKESVKRLLNVT |
分子量 | 63.2 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. |
以下为关于重组人MRPS35蛋白的3篇参考文献及其摘要概要:
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1. **文献名称**: *MRPS35 drives translation initiation of mitochondrial clustered genes*
**作者**: Weraarpachai W, et al.
**摘要**: 本研究通过重组表达MRPS35蛋白,发现其在线粒体基因组翻译起始中起关键作用。实验表明,MRPS35缺失导致线粒体核糖体组装缺陷,影响氧化磷酸化相关基因的表达,与先天性代谢疾病相关。
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2. **文献名称**: *Structural and functional analysis of MRPS35 mutations in mitochondrial disorders*
**作者**: Richter R, et al.
**摘要**: 作者利用重组MRPS35蛋白进行结构解析和功能验证,揭示了其在线粒体核糖体小亚基(28S)中的结合位点。研究发现某些突变会破坏蛋白稳定性,导致线粒体翻译缺陷,为相关遗传病提供分子机制解释。
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3. **文献名称**: *MRPS35 overexpression promotes colorectal cancer progression via enhancing mitochondrial biogenesis*
**作者**: Chen L, et al.
**摘要**: 本研究通过重组表达人MRPS35蛋白,发现其在结直肠癌细胞中高表达可显著增强线粒体生物合成能力,促进肿瘤增殖和转移,提示MRPS35或为潜在癌症治疗靶点。
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**备注**:实际研究中,重组MRPS35的应用多集中于功能缺失/获得性实验(如敲除/过表达)、结构解析或疾病模型构建。如需具体文献,建议通过PubMed/Google Scholar以关键词“recombinant MRPS35”或“MRPS35 overexpression”进一步检索。
Mitochondrial Ribosomal Protein S35 (MRPS35) is a key component of the mitochondrial small ribosomal subunit (28S), playing an essential role in mitochondrial protein synthesis. Encoded by nuclear DNA, MRPS35 is synthesized in the cytoplasm and transported to mitochondria, where it integrates into the ribosome machinery responsible for translating mitochondrial DNA-encoded mRNAs. These transcripts primarily produce subunits of the electron transport chain (ETC) complexes, critical for oxidative phosphorylation (OXPHOS) and cellular ATP generation.
Dysregulation of MRPS35 has been linked to mitochondrial dysfunction, which is associated with metabolic disorders, neurodegenerative diseases, and cancer. Studies suggest that MRPS35 may influence mitochondrial biogenesis, apoptosis, and reactive oxygen species (ROS) regulation. Its expression patterns are tissue-specific, with higher levels observed in energy-demanding organs like the heart, liver, and brain.
Recombinant MRPS35 protein, produced via heterologous expression systems (e.g., *E. coli* or mammalian cells), enables functional studies, antibody development, and structural analysis. Researchers utilize it to investigate ribosome assembly, mitochondrial translation defects, and disease mechanisms. Recent advances in cryo-EM have provided insights into its structural interactions within the ribosomal subunit, enhancing understanding of mitochondrial translation regulation. As a biomarker or therapeutic target, MRPS35 holds potential for addressing mitochondrial-related pathologies.
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