纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | SLITRK1 |
Uniprot No | Q96PX8 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 1-616aa |
氨基酸序列 | MLLWILLLET SLCFAAGNVT GDVCKEKICS CNEIEGDLHV DCEKKGFTSL QRFTAPTSQF YHLFLHGNSL TRLFPNEFAN FYNAVSLHME NNGLHEIVPG AFLGLQLVKR LHINNNKIKS FRKQTFLGLD DLEYLQADFN LLRDIDPGAF QDLNKLEVLI LNDNLISTLP ANVFQYVPIT HLDLRGNRLK TLPYEEVLEQ IPGIAEILLE DNPWDCTCDL LSLKEWLENI PKNALIGRVV CEAPTRLQGK DLNETTEQDL CPLKNRVDSS LPAPPAQEET FAPGPLPTPF KTNGQEDHAT PGSAPNGGTK IPGNWQIKIR PTAAIATGSS RNKPLANSLP CPGGCSCDHI PGSGLKMNCN NRNVSSLADL KPKLSNVQEL FLRDNKIHSI RKSHFVDYKN LILLDLGNNN IATVENNTFK NLLDLRWLYM DSNYLDTLSR EKFAGLQNLE YLNVEYNAIQ LILPGTFNAM PKLRILILNN NLLRSLPVDV FAGVSLSKLS LHNNYFMYLP VAGVLDQLTS IIQIDLHGNP WECSCTIVPF KQWAERLGSE VLMSDLKCET PVNFFRKDFM LLSNDEICPQ LYARISPTLT SHSKNSTGLA ETGTHSNSYL DTSRVS |
预测分子量 | 95 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SLITRK1重组蛋白的参考文献示例(注:部分信息为示例性虚构,仅供参考):
1. **《Recombinant SLITRK1 promotes synapse formation in cultured hippocampal neurons》**
- 作者:Smith A, et al.
- 摘要:研究通过在大肠杆菌中成功表达SLITRK1重组蛋白,并验证其在体外培养的海马神经元中促进突触形成的功能,表明SLITRK1在突触可塑性中的潜在作用。
2. **《SLITRK1 recombinant protein suppresses obsessive-compulsive behaviors in a murine model》**
- 作者:Lee B, et al.
- 摘要:利用哺乳动物细胞系统制备SLITRK1重组蛋白,发现其在小鼠模型中能够调节5-HT能系统,减轻强迫症样行为,为相关神经精神疾病的治疗提供依据。
3. **《Structural characterization of human SLITRK1 extracellular domain using recombinant protein expression》**
- 作者:Zhang C, et al.
- 摘要:通过昆虫细胞表达系统获得高纯度SLITRK1胞外域重组蛋白,结合X射线晶体学解析其三维结构,揭示其与配体结合的分子机制。
4. **《SLITRK1 mutations alter recombinant protein function in neurodevelopmental disorders》**
- 作者:Johnson D, et al.
- 摘要:分析携带SLITRK1基因突变的患者来源重组蛋白,发现特定突变导致蛋白分泌障碍及神经元黏附活性下降,提示突变与自闭症谱系障碍的关联性。
建议通过PubMed或Google Scholar以“SLITRK1 recombinant protein”为关键词检索最新文献以获取真实数据。
SLITRK1 is a member of the SLITRK family of transmembrane proteins, primarily expressed in neurons and implicated in regulating synaptic development and neural circuit formation. The SLITRK family (SLIT and NTRK-like proteins) shares structural homology with both Slit guidance ligands and neurotrophic tyrosine kinase receptors (NTRKs), featuring leucine-rich repeat (LRR) domains in their extracellular regions and a conserved intracellular domain. SLITRK1. encoded by the *SLITRK1* gene located on human chromosome 13q31.1. has gained attention due to its association with neuropsychiatric disorders, particularly Tourette syndrome, obsessive-compulsive disorder (OCD), and trichotillomania.
Functionally, SLITRK1 modulates excitatory and inhibitory synaptic transmission by interacting with postsynaptic proteins like receptor tyrosine phosphatases (e.g., PTPδ), influencing synaptic plasticity and stability. Studies in animal models suggest its role in dendritic growth, axonal guidance, and maintaining excitatory-inhibitory balance in neural networks. Dysregulation of SLITRK1 has been linked to altered synaptic connectivity, potentially contributing to behavioral phenotypes observed in neurodevelopmental disorders.
Recombinant SLITRK1 protein is engineered for *in vitro* and *in vivo* studies to dissect its molecular interactions, signaling pathways, and therapeutic potential. Produced via heterologous expression systems (e.g., mammalian or insect cells), the recombinant protein retains post-translational modifications critical for its biological activity. Researchers utilize it to investigate disease mechanisms, screen for small-molecule modulators, or develop antibody-based therapies targeting SLITRK1-associated pathways. Despite progress, its precise mechanistic roles and therapeutic applicability remain under active exploration, reflecting the complexity of synaptic regulation in neuropathologies.
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