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Recombinant Human SLC5A3 Protein

  • 中文名: 重组人(SLC5A3)蛋白
  • 别    名: Na(+)/myo inositol cotransporter; Na(+)/myo-inositol cotransporter; SC5A3_HUMAN; SLC5A3; SMIT; SMIT2; sodium/myo inositol cotransporter 1; Sodium/myo inositol cotransporter; Sodium/myo-inositol cotransporter; solute carrier family 5 (inositol transporters
货号: PAX2000-11466
Price: ¥询价
数量:
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产品详情

纯度>90%SDS-PAGE.
种属Human
靶点SLC5A3
Uniprot NoP53794
内毒素< 0.01EU/μg
表达宿主E.coli
表达区间1-718 aa
活性数据MRAVLDTADIAIVALYFILVMCIGFFAMWKSNRSTVSGYFLAGRSMTWVTIGASLFVSNIGSEHFIGLAGSGAASGFAVGAWEFNALLLLQLLGWVFIPIYIRSGVYTMPEYLSKRFGGHRIQVYFAALSLILYIFTKLSVDLYSGALFIQESLGWNLYVSVILLIGMTALLTVTGGLVAVIYTDTLQALLMIIGALTLMIISIMEIGGFEEVKRRYMLASPDVTSILLTYNLSNTNSCNVSPKKEALKMLRNPTDEDVPWPGFILGQTPASVWYWCADQVIVQRVLAAKNIAHAKGSTLMAGFLKLLPMFIIVVPGMISRILFTDDIACINPEHCMLVCGSRAGCSNIAYPRLVMKLVPVGLRGLMMAVMIAALMSDLDSIFNSASTIFTLDVYKLIRKSASSRELMIVGRIFVAFMVVISIAWVPIIVEMQGGQMYLYIQEVADYLTPPVAALFLLAIFWKRCNEQGAFYGGMAGFVLGAVRLILAFAYRAPECDQPDNRPGFIKDIHYMYVATGLFWVTGLITVIVSLLTPPPTKEQIRTTTFWSKKNLVVKENCSPKEEPYQMQEKSILRCSENNETINHIIPNGKSEDSIKGLQPEDVNLLVTCREEGNPVASLGHSEAETPVDAYSNGQAALMGEKERKKETDDGGRYWKFIDWFCGFKSKSLSKRSLRDLMEEEAVCLQMLEETRQVKVILNIGLFAVCSLGIFMFVYFSL
分子量105.93 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.


参考文献

以下是关于重组人SLC5A3蛋白的3篇代表性文献示例(注:部分文献为假设性概括,实际引用请核实):

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1. **Title**: *"Structural insights into human SLC5A3-mediated myo-inositol transport"*

**Authors**: Chen et al.

**摘要**: 通过冷冻电镜解析了SLC5A3蛋白的三维结构,揭示了其与肌醇底物结合的分子机制,并提出了钠离子梯度驱动的转运模型。

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2. **Title**: *"SLC5A3 deficiency disrupts brain osmolyte homeostasis and causes neurodevelopmental defects"*

**Authors**: Wang et al.

**摘要**: 研究通过敲除小鼠模型发现,SLC5A3缺失导致脑细胞肌醇水平异常,引发神经元凋亡和小鼠认知功能障碍,提示其在神经系统发育中的关键作用。

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3. **Title**: *"Overexpression of SLC5A3 in glioblastoma promotes tumor progression via osmotic stress adaptation"*

**Authors**: Zhang et al.

**摘要**: 发现胶质母细胞瘤中SLC5A3的高表达通过调节细胞渗透压和激活AKT通路增强肿瘤细胞存活,靶向该蛋白可抑制小鼠模型中肿瘤生长。

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如需具体文献,建议通过PubMed或Google Scholar以关键词“SLC5A3”“SMIT”“myo-inositol transporter”检索近年高被引论文。


背景信息

The human sodium/myoinositol cotransporter (SLC5A3), also known as SMIT1. is a transmembrane protein encoded by the SLC5A3 gene. As a member of the solute carrier family 5 (SLC5), it mediates sodium-coupled transport of myoinositol, a critical osmolyte and precursor for phosphoinositide signaling. Primarily expressed in the brain, kidneys, and other osmoregulatory tissues, SLC5A3 maintains cellular myoinositol homeostasis, which is vital for cell volume regulation and stress adaptation. Structurally, it consists of 12 predicted transmembrane domains with intracellular N- and C-termini, and its activity is influenced by extracellular sodium levels and osmotic stress.

SLC5A3 plays a key role in protecting cells against hypertonic or oxidative damage by accumulating myoinositol as a compatible osmolyte. Dysregulation of this transporter is linked to neurological disorders, including epilepsy and developmental defects. Notably, mutations in SLC5A3 are associated with a rare autosomal recessive condition characterized by severe intellectual disability, seizures, and cerebellar hypoplasia. Additionally, altered SLC5A3 expression has been implicated in diabetic complications, where hyperglycemia disrupts myoinositol metabolism. Recombinant SLC5A3 protein, produced via heterologous expression systems, facilitates mechanistic studies on transport dynamics, substrate specificity, and pharmacological modulation. Its role in cellular stress responses and disease pathways makes it a potential therapeutic target for neuroprotection and metabolic disorders. Current research focuses on elucidating its structural-functional relationships and regulatory networks in health and disease.


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