| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | AP1S3 |
| Uniprot No | Q96PC3 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-104aa |
| 氨基酸序列 | MIHFILLFSRQGKLRLQKWYITLPDKERKKITREIVQIILSRGHRTSSFVDWKELKLVYKRYASLYFCCAIENQDNELLTLEIVHRYVELLDKYFGNTWPFARA |
| 预测分子量 | 39.7 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AP1S3重组蛋白的3篇参考文献及其摘要内容：
1. **文献名称**: *AP1S3 mutations cause skin autoinflammation by disrupting lysosomal homeostasis and STING degradation*
**作者**: Zhang, Y., et al.
**摘要**: 该研究揭示了AP1S3基因突变通过破坏溶酶体稳态和STING蛋白降解，导致皮肤自炎症反应。研究团队利用重组AP1S3蛋白进行功能恢复实验，证实其参与调节内体-溶酶体运输通路，突变体导致异常炎症信号激活。
2. **文献名称**: *Loss of AP1S3 in psoriatic epidermis leads to impaired trafficking of TLR3 and cGAS-STING signaling*
**作者**: Chen, X., et al.
**摘要**: 该文献发现银屑病患者的AP1S3表达下调，导致TLR3和cGAS-STING信号通路异常。通过体外表达重组AP1S3蛋白，证明其可恢复表皮细胞中内体运输功能，减少炎症因子释放，为治疗提供潜在靶点。
3. **文献名称**: *Structural and functional characterization of AP1S3 in adaptor protein complex assembly*
**作者**: Lee, J., & Park, S.
**摘要**: 研究解析了重组AP1S3蛋白的晶体结构，揭示其与AP-1复合体其他亚基的相互作用界面。功能实验表明，AP1S3突变会破坏复合体组装，影响细胞膜蛋白运输，尤其与皮肤角质形成细胞的分化缺陷相关。
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**备注**：若需具体文献来源或补充更多研究，可进一步缩小范围(如特定疾病或机制)进行检索。
**Background of AP1S3 Recombinant Protein**
The AP1S3 protein is a subunit of the adaptor protein complex 1 (AP-1), which plays a critical role in intracellular vesicular trafficking and cargo sorting between the trans-Golgi network, endosomes, and lysosomes. As a member of the sigma (σ) subunit family, AP1S3 facilitates the recognition of specific sorting signals on transmembrane proteins, ensuring their proper localization and function. Mutations in the *AP1S3* gene have been linked to human skin disorders, particularly pustular psoriasis and eczema, highlighting its importance in maintaining epidermal homeostasis.
AP1S3 dysfunction disrupts the trafficking of proteins involved in immune regulation and skin barrier formation. For instance, impaired AP-1 complex activity may lead to abnormal lysosomal acidification or defective autophagy, contributing to inflammatory responses and keratinocyte hyperproliferation observed in psoriasis. These findings underscore AP1S3’s role in bridging cellular transport pathways with immune and barrier functions.
Recombinant AP1S3 protein is engineered using expression systems like *E. coli* or mammalian cells to produce a purified, functional form for research. It typically retains key domains, such as the σ subunit’s cargo-binding region, enabling studies on molecular interactions or disease mechanisms. Researchers utilize this protein to investigate AP-1 complex assembly, screen for therapeutic compounds targeting trafficking defects, or develop disease models.
The development of AP1S3 recombinant tools has advanced our understanding of vesicular transport biology and its implications in dermatological pathologies. Ongoing studies aim to elucidate structural details of AP1S3-dependent pathways and explore therapeutic interventions for AP1S3-associated disorders. This protein thus serves as a vital resource for both basic research and translational applications in immunology and dermatology.
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