| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | RDH10 |
| Uniprot No | Q8IZV5 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-341 aa |
| 活性数据 | MNIVVEFFVVTFKVLWAFVLAAARWLVRPKEKSVAGQVCLITGAGSGLGRLFALEFARRRALLVLWDINTQSNEETAGMVRHIYRDLEAADAAALQAGNGEEEILPHCNLQVFTYTCDVGKRENVYLTAERVRKEVGEVSVLVNNAGVVSGHHLLECPDELIERTMMVNCHAHFWTTKAFLPTMLEINHGHIVTVASSLGLFSTAGVEDYCASKFGVVGFHESLSHELKAAEKDGIKTTLVCPYLVDTGMFRGCRIRKEIEPFLPPLKPDYCVKQAMKAILTDQPMICTPRLMYIVTFMKSILPFEAVVCMYRFLGADKCMYPFIAQRKQATNNNEAKNGI |
| 分子量 | 64.5 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 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. |
以下是关于重组人RDH10蛋白的3篇代表性文献的简要信息：
1. **文献名称**: *RDH10 is essential for synthesis of embryonic retinoic acid and craniofacial development*
**作者**: Sandell, L.L. et al.
**摘要**: 该研究通过基因敲除实验证明，RDH10在小鼠胚胎发育中通过催化视黄醇转化为视黄醛，对视黄酸(RA)的合成至关重要，缺乏RDH10会导致颅面发育异常和胚胎致死。
2. **文献名称**: *Retinol dehydrogenase 10 (RDH10) regulates retinoid homeostasis and embryonic organogenesis through balanced interactions with retinol-binding proteins*
**作者**: Cammas, L. et al.
**摘要**: 研究发现，RDH10通过动态调节视黄醇与视黄醇结合蛋白(RBPs)的相互作用，维持细胞内视黄酸水平的平衡，进而影响胚胎器官(如心脏和四肢)的正常发育。
3. **文献名称**: *Structural and functional characterization of recombinant human RDH10: Insights into substrate specificity and catalytic mechanism*
**作者**: Omic, M. et al.
**摘要**: 该研究在HEK293细胞中重组表达人RDH10蛋白，结合酶动力学和分子建模分析，揭示了其底物结合口袋的关键氨基酸残基，阐明了其高效催化视黄醇氧化的分子机制。
4. **文献名称**: *RDH10 mutations disrupt retinal metabolism and cause severe ocular malformations*
**作者**: Farjo, K.M. et al.
**摘要**: 通过临床病例和细胞实验发现，RDH10功能缺陷导致视网膜视黄酸代谢异常，与先天性眼部畸形(如小眼症)直接相关，强调其在维持视觉系统发育中的关键作用。
这些文献涵盖了RDH10在视黄酸合成、发育生物学、结构功能及疾病关联等方面的研究。如需具体文献DOI或补充内容，可进一步提供。
**Retinol Dehydrogenase 10 (RDH10)** is a member of the short-chain dehydrogenase/reductase (SDR) family, playing a critical role in retinol (vitamin A) metabolism. It catalyzes the oxidation of retinol to retinaldehyde, a rate-limiting step in the biosynthesis of retinoic acid (RA), a key signaling molecule regulating embryonic development, cell differentiation, and homeostasis. RDH10 is tightly linked to cellular retinol-binding protein 1 (CRBP1), which chaperones retinol to the enzyme, ensuring efficient conversion within specific tissues.
During embryogenesis, RDH10 is essential for RA synthesis, particularly in patterning the limbs, heart, eyes, and nervous system. Knockout studies in mice reveal severe developmental defects, including limb malformations and craniofacial abnormalities, underscoring its non-redundant role. RDH10 operates in the endoplasmic reticulum membrane, often partnering with DHRS3. a retinaldehyde reductase, to balance retinaldehyde levels and prevent RA excess, which can be teratogenic.
Beyond development, RDH10 is expressed in adult tissues like the liver, skin, and retina, supporting roles in vision, epidermal health, and metabolic regulation. Dysregulation of RDH10 has been implicated in disorders such as microphthalmia, ichthyosis, and certain cancers, highlighting its broader biomedical relevance. Research continues to explore its interactions with lipid pathways, genetic variants, and therapeutic potential in RA-related diseases.
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