| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | LRBA |
| Uniprot No | P50851 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1267-1500aa |
| 氨基酸序列 | PQPHRHVLEISRQHEQPGQGIAPDAVNGQRRDSRSTVFRIPEFNWSQMHQRLLTDLLFSIETDIQMWRSHSTKTVMDFVNSSDNVIFVHNTIHLISQVMDNMVMACGGILPLLSAATSATHELENIEPTQGLSIEASVTFLQRLISLVDVLIFASSLGFTEIEAEKSMSSGGILRQCLRLVCAVAVRNCLECQQHSQLKTRGDKALKPMHSLIPLGKSAAKSPVDIVTGGISPV |
| 预测分子量 | 29.8 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LRBA(LPS-responsive beige-like anchor protein)重组蛋白的3篇文献摘要概括，基于模拟数据整理：
---
1. **文献名称**：*LRBA regulates autophagy and lysosome function in immune cells*
**作者**：Lo B et al.
**摘要**：研究通过构建重组LRBA蛋白，揭示了其在免疫细胞中调控自噬体和溶酶体融合的分子机制，发现LRBA缺失导致溶酶体功能异常和自身免疫表型。
2. **文献名称**：*Structural insights into LRBA-mediated vesicle trafficking*
**作者**：Zhang Y et al.
**摘要**：利用重组LRBA蛋白进行X射线晶体学分析，解析其PH结构域与细胞膜磷脂相互作用的分子基础，阐明其在胞内囊泡运输中的关键作用。
3. **文献名称**：*LRBA deficiency corrected by recombinant protein therapy in a murine model*
**作者**：Alazami AM et al.
**摘要**：在小鼠模型中，通过递送重组LRBA蛋白成功恢复免疫细胞功能，为LRBA缺陷相关免疫失调疾病的治疗提供了实验依据。
---
注：以上文献信息为示例性概括，实际文献需通过PubMed或专业数据库检索确认。
LRBA (LPS-responsive vesicular trafficking regulator and beacon) is a large, multidomain protein encoded by the *LRBA* gene, primarily involved in regulating intracellular vesicular trafficking and immune homeostasis. Structurally, LRBA contains multiple functional domains, including ARM (Armadillo), BEACH (BEige And Chediak-Higashi), WD40 repeats, and pleckstrin homology (PH) domains, which enable interactions with membranes, proteins, and signaling molecules. It plays a critical role in maintaining the dynamic balance of cellular organelles, such as the Golgi apparatus, endosomes, and lysosomes, by modulating vesicle transport and receptor recycling.
LRBA gained prominence due to its connection with immune regulation. It regulates the expression of CTLA-4. a key immune checkpoint protein that suppresses T-cell activation. LRBA prevents CTLA-4 degradation by sequestering it in recycling endosomes, ensuring its availability on regulatory T cells (Tregs) and activated effector T cells. Mutations in *LRBA* cause LRBA deficiency, a rare autosomal recessive disorder characterized by immune dysregulation, including common variable immunodeficiency (CVID), autoimmune cytopenias, enteropathy, and lymphoproliferation. Patients often exhibit reduced CTLA-4 levels, leading to unchecked immune activation and autoimmunity.
Beyond immunity, LRBA is implicated in cancer, neurodevelopment, and metabolic processes. Its broad tissue expression underscores its role in cellular homeostasis. Research on LRBA has spurred therapeutic innovations, such as CTLA-4 replacement therapies (e.g., abatacept) and targeted molecular interventions, highlighting its potential as a biomarker or therapeutic target for immune-related diseases. Ongoing studies aim to unravel its precise mechanisms in vesicular dynamics and cross-talk with other trafficking regulators like CHS1/LYST.
×
