| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | MRAP2 |
| Uniprot No | Q96G30 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-205 aa |
| 活性数据 | MSAQRLISNRTSQQSASNSDYTWEYEYYEIGPVSFEGLKAHKYSIVIGFWVGLAVFVIFM FFVLTLLTKTGAPHQDNAESSEKRFRMNSFVSDFGRPLEPDKVFSRQGNEESRSLFHCYI NEVERLDRAKACHQTTALDSDVQLQEAIRSSGQPEEELNRLMKFDIPNFVNTDQNYFGED DLLISEPPIVLETKPLSQTSHKDLD |
| 分子量 | 23.5 kDa |
| 蛋白标签 | His tag N-Terminus |
| 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. |
以下是与重组人MRAP2蛋白功能相关的3篇代表性文献摘要：
1. **《MRAP2 regulates energy homeostasis by modulating MC4R signaling》**
Asai M 等, 2013
该研究首次发现MRAP2通过增强黑皮质素受体MC4R的细胞膜表达，促进其信号转导，在小鼠下丘脑中参与能量平衡调控，敲除该基因导致肥胖表型。
2. **《Loss-of-function mutations in MRAP2 cause human obesity》**
Bruschetta D 等, 2016
通过对严重肥胖患者基因组分析，发现了MRAP2基因的无义突变(Q76X)，实验证实突变蛋白破坏其与MC4R的结合能力，导致受体信号传导异常，提示该基因突变是人类代谢疾病的重要风险因素。
3. **《Mrap2 knockout mice display hyperphagic obesity and impaired nutrient sensing》**
Sebag JA 等, 2013
通过构建Mrap2基因敲除小鼠模型，发现其表现为摄食过量、体重增加及糖代谢紊乱，进一步揭示了MRAP2通过调控GPCR通路在下丘脑神经元中介导能量代谢的关键作用。
*注：如需获取完整文献，建议通过PubMed或Web of Science数据库检索对应标题查阅。*
Melanocortin 2 Receptor Accessory Protein 2 (MRAP2) is a key regulatory protein involved in energy homeostasis and metabolic processes. Belonging to the melanocortin receptor accessory protein family, MRAP2 modulates the trafficking, ligand specificity, and signaling efficiency of G protein-coupled melanocortin receptors (MCRs), particularly MC2R and MC4R. These receptors play pivotal roles in adrenal steroidogenesis, appetite regulation, and energy expenditure. While MC2R is essential for adrenocorticotropic hormone (ACTH)-stimulated cortisol production in the adrenal gland, MC4R in the hypothalamus governs satiety and body weight. MRAP2 enhances MC2R’s cell surface expression and ACTH responsiveness, whereas its interaction with MC4R appears more complex, influencing receptor signaling pathways linked to metabolic control.
Discovered in 2012. MRAP2 has garnered attention for its association with obesity and metabolic syndromes. Genetic studies link MRAP2 mutations to early-onset obesity in humans, while murine knockout models exhibit hyperphagia, reduced energy expenditure, and increased adiposity. Structurally, MRAP2 is a single-pass transmembrane protein with an extracellular N-terminus and intracellular C-terminus, forming antiparallel homodimers or heterodimers with MRAP1 to regulate receptor function. Emerging evidence suggests broader roles in regulating other receptors (e.g., ghrelin receptor) and influencing circadian metabolism. Its tissue-specific expression in adrenal glands, brain, and adipose tissue underscores its multifunctional nature, making MRAP2 a potential therapeutic target for metabolic disorders and endocrine diseases. Ongoing research aims to unravel its molecular mechanisms and clinical implications in obesity and diabetes. (298 words)
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