| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | SLC6A5 |
| Uniprot No | Q9Y345 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 294-393 aa |
| 活性数据 | TLFYLFASFVSVLPWGSCNNPWNTPECKDKTKLLLDSCVISDHPKIQIKNSTFCMTAYPNVTMVNFTSQANKTFVSGSEEYFKYFVLKISAGIEYPGEIR |
| 分子量 | 36.74 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. |
以下为3条关于重组人SLC6A5(GlyT2)蛋白的参考文献示例：
1. **文献名称**: *"Functional Characterization of Recombinant Human GlyT2 (SLC6A5) in Mammalian Cells for Inhibitor Screening"*
**作者**: Smith A et al.
**摘要**: 研究报道了在HEK293细胞中重组表达人源SLC6A5蛋白，并通过放射性同位素标记验证其甘氨酸转运活性，建立高通量筛选模型用于发现新型GlyT2抑制剂，为神经痛治疗药物开发提供平台。
2. **文献名称**: *"Crystal Structure of the Human GlyT2 Transporter Reveals Mechanisms of Substrate Recognition"*
**作者**: Chen L et al.
**摘要**: 首次解析了重组人SLC6A5蛋白的晶体结构(分辨率为3.0 Å)，揭示其甘氨酸结合域的关键氨基酸残基及构象变化，阐明选择性运输甘氨酸的分子机制，为靶向药物设计提供结构基础。
3. **文献名称**: *"Role of Recombinant SLC6A5 in Hyperekplexia: Electrophysiological Analysis in Xenopus Oocytes"*
**作者**: Kimura T et al.
**摘要**: 通过在非洲爪蟾卵母细胞中表达重组SLC6A5蛋白，结合电生理学实验证明其功能缺失突变导致甘氨酸再摄取障碍，解释了遗传性过度惊厥症(hyperekplexia)的病理机制，并提出突变修复策略。
注：以上文献为示例性内容，实际引用需根据具体研究查找真实文献。
The human SLC6A5 protein, also known as glycine transporter 2 (GlyT2), is a key player in inhibitory neurotransmission. Belonging to the solute carrier 6 (SLC6) family, it primarily functions to regulate synaptic glycine levels by reabsorbing glycine from the synaptic cleft into presynaptic neurons, particularly in the brainstem and spinal cord. This Na⁺/Cl⁻-dependent transporter is critical for maintaining glycinergic signaling, which modulates motor coordination, pain perception, and respiratory rhythms.
Structurally, SLC6A5 contains 12 transmembrane domains with intracellular N- and C-termini. Its dysfunction is linked to neurological disorders. Autosomal recessive mutations in SLC6A5 cause hyperekplexia (startle disease), characterized by exaggerated startle reflexes and muscle rigidity, due to impaired glycine clearance and disrupted inhibitory neurotransmission. Conversely, excessive GlyT2 activity may contribute to chronic pain, making it a therapeutic target.
Recombinant SLC6A5 proteins are produced using heterologous expression systems (e.g., HEK293 cells, baculovirus) for structural and functional studies. These tools enable research on transport mechanisms, ligand interactions, and drug discovery. Inhibitors targeting GlyT2. such as ORG-25543. are explored as potential analgesics. However, challenges remain in achieving selectivity over the closely related GlyT1 isoform. Advances in cryo-EM and molecular dynamics simulations are enhancing mechanistic understanding, guiding the development of precision therapeutics for neurological and pain-related conditions.
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