纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | Mkrn3 |
Uniprot No | P31947 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 1-248aa |
氨基酸序列 | MERASLIQKAKLAEQAERYEDMAAFMKGAVEKGEELSCEERNLLSVAYKNVVGGQRAAWRVLSSIEQKSNEEGSEEKGPEVREYREKVETELQGVCDTVLGLLDSHLIKEAGDAESRVFYLKMKGDYYRYLAEVATGDDKKRIIDSARSAYQEAMDISKKEMPPTNPIRLGLALNFSVFHYEIANSPEEAISLAKTTFDEAMADLHTLSEDSYKDSTLIMQLLRDNLTLWTADNAGEEGGEAPQEPQS |
预测分子量 | 54.8kDa |
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Mkrn3重组蛋白的模拟参考文献示例(非真实文献,仅供格式参考):
1. **"Functional Characterization of Recombinant Mkrn3 Protein in Neuronal Development"**
*Author: Smith A, et al.*
**摘要**:本研究通过体外表达重组Mkrn3蛋白,发现其通过泛素化途径调控突触蛋白降解,影响小鼠神经元突触可塑性,提示Mkrn3在神经发育中的潜在作用。
2. **"Mkrn3 Recombinant Protein Rescues Imprinting Defects in Prader-Willi Syndrome Models"**
*Author: Lee J, et al.*
**摘要**:利用重组Mkrn3蛋白处理Prader-Willi综合征细胞模型,观察到部分印记基因表达恢复,表明Mkrn3可能在表观遗传调控中起关键作用。
3. **"Expression and Purification of Bioactive Mkrn3 Recombinant Protein in E. coli"**
*Author: Chen X, et al.*
**摘要**:报道了一种高效的大肠杆菌表达系统,成功获得高纯度Mkrn3重组蛋白,并通过体外实验验证其结合RNA及泛素连接酶活性。
4. **"Mkrn3 Knockdown and Recombinant Protein Supplementation in Puberty Timing Regulation"**
*Author: García-Ruiz G, et al.*
**摘要**:动物实验表明,重组Mkrn3蛋白可逆转下丘脑神经元中促性腺激素释放激素的异常分泌,为中枢性性早熟机制提供新见解。
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**注意**:以上为模拟示例,实际文献需通过PubMed/Google Scholar等平台检索关键词(如“Mkrn3 recombinant protein”、“MKRN3 function”)获取。真实研究多聚焦于Mkrn3在印记基因调控、神经内分泌疾病及泛素化通路中的作用。
Mkrn3 (Makorin Ring Finger Protein 3) is a member of the makorin family of proteins characterized by the presence of a distinctive RING finger domain, which is often associated with ubiquitin ligase activity and protein-protein interactions. The gene encoding Mkrn3 is located in the Prader-Willi syndrome (PWS) critical region on human chromosome 15q11-q13. an imprinted region linked to neurodevelopmental disorders. Mkrn3 is paternally expressed, and its loss or mutation has been implicated in central precocious puberty (CPP), a condition marked by early activation of the hypothalamic-pituitary-gonadal axis. This connection was highlighted by studies showing that paternal mutations or deletions in MKRN3 lead to premature puberty, suggesting its role as a key inhibitor of reproductive axis activation during childhood.
Functionally, Mkrn3 is thought to participate in ubiquitination pathways, potentially regulating protein turnover or signaling cascades. Its RING domain may mediate interactions with substrates for proteasomal degradation, though specific targets remain under investigation. Additionally, Mkrn3 has been associated with RNA metabolism and translational control, indicating broader roles in post-transcriptional regulation. Recombinant Mkrn3 protein, produced via expression systems like E. coli or mammalian cells, enables in vitro studies to dissect its biochemical properties, interaction networks, and enzymatic activities. Researchers employ such tools to explore its regulatory mechanisms in puberty, neurodevelopment, and imprinting disorders.
Beyond reproductive biology, Mkrn3 is studied in cancer due to its dysregulation in tumors, though its role as an oncogene or tumor suppressor remains context-dependent. The development of recombinant Mkrn3 has accelerated structural studies, antibody production, and functional assays, offering insights into its dual roles in physiology and disease. Ongoing research aims to clarify its molecular targets and therapeutic potential, particularly in puberty-related disorders and imprinting syndromes like PWS.
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