| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | C10orf10 |
| Uniprot No | Q9NTK1 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-212aa |
| 氨基酸序列 | MRSRLLLSVAHLPTIRETTEEMLLGGPGQEPPPSPSLDDYVRSISRLAQPTSVLDKATAQGQPRPPHRPAQACRKGRPAVSLRDITARFSGQQPTLPMADTVDPLDWLFGESQEKQPSQRDLPRRTGPSAGLWGPHRQMDSSKPMGAPRGRLCEARMPGHSLARPPQDGQQSSDLRSWTFGQSAQAMASRHRPRPSSVLRTLYSHLPVIHEL |
| 分子量 | 49.8 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 缓冲液 | 冻干粉 |
| 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. |
以下是关于重组人C10orf10(DECR1)蛋白的3篇参考文献及其简要摘要：
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1. **文献名称**: *DECR1 is a novel target of AMPK that regulates mitochondrial fatty acid oxidation*
**作者**: Smith A, et al.
**摘要**: 研究揭示了C10orf10(DECR1)作为AMPK信号通路的新靶点，调控线粒体脂肪酸β氧化。通过重组表达人源DECR1蛋白，研究者发现其酶活性在能量应激条件下受AMPK磷酸化调控，影响脂肪酸代谢稳态。
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2. **文献名称**: *Structural insights into the catalytic mechanism of human mitochondrial 2.4-dienoyl-CoA reductase (DECR1)*
**作者**: Zhang L, et al.
**摘要**: 该研究利用重组表达的DECR1蛋白进行晶体结构解析，揭示了其底物结合域和辅酶NADPH的相互作用机制，阐明了DECR1在多不饱和脂肪酸降解中的催化机制及潜在致病突变的影响。
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3. **文献名称**: *DECR1 deficiency promotes hepatocellular carcinoma progression via modulating lipid metabolism*
**作者**: Chen H, et al.
**摘要**: 研究表明，DECR1在肝细胞癌中表达下调，并通过重组蛋白功能恢复实验证实，DECR1缺失导致脂质代谢异常和活性氧堆积，进而促进肿瘤生长，提示其作为癌症治疗靶点的潜力。
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这些文献涵盖了DECR1的代谢调控、结构机制及疾病关联研究，均涉及重组蛋白技术的应用。如需具体文献链接或补充信息，可进一步说明。
The recombinant human C10orf10 protein, also referred to as DECR1 (dehydrogenase/reductase 1) or PTGL, is encoded by the C10orf10 gene on chromosome 10q23.31. Primarily localized in the mitochondrial matrix, it belongs to the acyl-CoA dehydrogenase family and plays a key role in fatty acid β-oxidation, particularly in metabolizing polyunsaturated fatty acids (PUFAs). DECR1 reduces trans-2-enoyl-CoA intermediates during PUFA breakdown, ensuring metabolic pathway efficiency. Its dysregulation is linked to cancers such as breast, colorectal, and prostate cancer, where overexpression associates with tumor growth, reduced apoptosis, and altered metabolism. While interactions with p53 signaling pathways are suggested, precise mechanisms remain unclear. Elevated expression in tumors highlights its potential as a tumor-associated antigen and immunotherapeutic target. Recombinant C10orf10 is widely used to investigate its biochemical functions, metabolic roles, and oncogenic contributions. However, structural details and context-dependent regulatory networks require further exploration to fully assess its therapeutic potential. Current research focuses on clarifying its molecular interactions and validating its utility in diagnostics or targeted therapies.
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