纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | MYLIP |
Uniprot No | Q8WY64 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 1-445aa |
氨基酸序列 | MLCYVTRPDAVLMEVEVEAKANGEDCLNQVCRRLGIIEVDYFGLQFTGSKGESLWLNLRNRISQQMDGLAPYRLKLRVKFFVEPHLILQEQTRHIFFLHIKEALLAGHLLCSPEQAVELSALLAQTKFGDYNQNTAKYNYEELCAKELSSATLNSIVAKHKELEGTSQASAEYQVLQIVSAMENYGIEWHSVRDSEGQKLLIGVGPEGISICKDDFSPINRIAYPVVQMATQSGKNVYLTVTKESGNSIVLLFKMISTRAASGLYRAITETHAFYRCDTVTSAVMMQYSRDLKGHLASLFLNENINLGKKYVFDIKRTSKEVYDHARRALYNAGVVDLVSRNNQSPSHSPLKSSESSMNCSSCEGLSCQQTRVLQEKLRKLKEAMLCMVCCEEEINSTFCPCGHTVCCESCAAQLQSCPVCRSRVEHVQHVYLPTHTSLLNLTVI |
预测分子量 | 51.9 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MYLIP重组蛋白的3篇虚构参考文献示例(内容基于领域常识编排,非真实文献):
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1. **文献名称**:*Structural and Functional Characterization of MYLIP as an E3 Ubiquitin Ligase*
**作者**:Zhang Y. et al.
**摘要**:本研究解析了MYLIP重组蛋白的晶体结构,揭示了其与E2泛素结合酶相互作用的关键结构域。实验表明,MYLIP通过泛素化修饰促进LDLR的降解,并证实其活性依赖于特定的锌指结构域。
2. **文献名称**:*MYLIP-Mediated LDL Receptor Regulation in Cholesterol Homeostasis*
**作者**:Hobbs H.H. & Cohen J.C.
**摘要**:文章通过体外重组蛋白实验和细胞模型,证明MYLIP受SREBP-2通路转录调控,并负反馈抑制LDLR的细胞表面表达,从而影响胆固醇摄取。敲除MYLIP可显著提高肝细胞LDLR水平。
3. **文献名称**:*In Vivo Role of MYLIP in Atherosclerosis Development*
**作者**:Fisher E.A. et al.
**摘要**:利用转基因小鼠模型,研究发现过表达MYLIP重组蛋白会加速动脉粥样硬化斑块形成,而抑制剂干预可逆转表型。结果表明MYLIP是胆固醇代谢和心血管疾病的潜在治疗靶点。
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注:以上文献为示例性质,实际研究中请以真实数据库(如PubMed)检索为准。
MYLIP (myosin regulatory light chain interacting protein), also known as IDOL (inducible degrader of the LDL receptor), is an E3 ubiquitin ligase encoded by the *MYLIP* gene located on human chromosome 6p22.3. It plays a critical role in cholesterol homeostasis by promoting the ubiquitination and subsequent degradation of the low-density lipoprotein receptor (LDLR), a key regulator of circulating cholesterol levels. MYLIP/IDOL is transcriptionally regulated by liver X receptors (LXRs), nuclear receptors that sense cellular cholesterol levels. When intracellular cholesterol accumulates, LXR activation induces MYLIP expression, leading to LDLR degradation and reduced cholesterol uptake—a feedback mechanism to prevent excessive cellular cholesterol accumulation.
The recombinant MYLIP protein, typically produced in bacterial or mammalian expression systems, retains its functional RING domain required for E3 ligase activity. Researchers use it to study LDLR regulation, lipid metabolism pathways, and potential therapeutic strategies for hypercholesterolemia. Its role in modulating LDLR independently of the PCSK9 pathway has sparked interest in developing MYLIP-targeted therapies, particularly for patients resistant to existing cholesterol-lowering drugs like statins or PCSK9 inhibitors. Additionally, MYLIP’s interaction with neuronal proteins implicates it in neurodegenerative disorders, broadening its research relevance. Purified recombinant MYLIP often includes tags (e.g., His-tag) for easier detection and isolation in biochemical assays, enabling studies on protein-protein interactions, ubiquitination mechanisms, and high-throughput drug screening.
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