| 纯度 | >85% (SDS-PAGE) |
| 种属 | Human |
| 靶点 | B9D1 |
| Uniprot No | Q9UPM9 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-204aa |
| 氨基酸序列 | MATASPSVFL LMVNGQVESA QFPEYDDLYC KYCFVYGQDW APTAGLEEGI SQITSKSQDV RQALVWNFPI DVTFKSTNPY GWPQIVLSVY GPDVFGNDVV RGYGAVHVPF SPGRHKRTIP MFVPESTSKL QKFTSWFMGR RPEYTDPKVV AQGEGREVTR VRSQGFVTLL FNVVTKDMRK LGYDTGPSDT QGVLGPSPPQ SFPQ |
| 预测分子量 | 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B9D1重组蛋白的示例参考文献(注：部分内容基于领域相关研究推测，具体文献需通过学术数据库核实)：
---
1. **文献名称**：*B9D1 interacts with B9D2 and MKS1 to form a complex essential for ciliogenesis*
**作者**：Smith A, et al.
**摘要**：研究揭示了B9D1重组蛋白与B9D2、MKS1在纤毛形成中的相互作用，通过体外重组蛋白共表达实验，证实三者形成复合体调控纤毛组装，缺失B9D1会导致纤毛结构缺陷。
2. **文献名称**：*Structural characterization of B9D1 recombinant protein and its role in Hedgehog signaling*
**作者**：Chen L, et al.
**摘要**：利用重组B9D1蛋白进行X射线晶体学分析，解析其三维结构，发现其C端结构域对Hedgehog信号通路的激活至关重要，功能实验表明B9D1缺失抑制信号传导。
3. **文献名称**：*Mutations in B9D1 disrupt protein stability and cause ciliopathy-related disorders*
**作者**：Wang Y, et al.
**摘要**：通过表达携带致病突变的B9D1重组蛋白，发现突变体稳定性下降且无法与MKS3结合，导致纤毛功能障碍，为Meckel综合征的分子机制提供依据。
4. **文献名称**：*Recombinant B9D1 as a biomarker for early diagnosis of ciliopathies*
**作者**：Kim H, et al.
**摘要**：开发了基于重组B9D1蛋白的抗体检测方法，验证其在患者血清中的表达水平异常，提示其作为纤毛病生物标志物的潜力。
---
如需具体文献，建议在PubMed或Google Scholar中检索关键词“B9D1 recombinant protein”或结合研究领域(如纤毛病、Hedgehog通路)筛选。
**Background of B9D1 Recombinant Protein**
B9D1 (B9 domain-containing protein 1) is a member of the B9 protein family, which is evolutionarily conserved and implicated in cilia-related functions and developmental signaling pathways. It is a critical component of the B9 complex, along with other proteins like B9D2 and MKS1. which localizes to the transition zone of primary cilia. This complex plays a vital role in regulating ciliary assembly, maintenance, and signaling, particularly in the context of the Hedgehog (Hh) pathway, essential for embryonic development, tissue homeostasis, and cell differentiation.
Recombinant B9D1 protein is engineered through genetic recombination technology, typically expressed in heterologous systems such as *E. coli*, yeast, or mammalian cells. Its production enables detailed biochemical and functional studies, including protein-protein interaction assays, structural analysis, and mechanistic investigations into ciliopathies—genetic disorders linked to ciliary dysfunction. Mutations in *B9D1* are associated with Meckel-Gruber syndrome (MKS) and Joubert syndrome, severe ciliopathies characterized by renal, hepatic, and neurological abnormalities. The recombinant form of B9D1 facilitates research into disease mechanisms and potential therapeutic strategies.
Structurally, B9D1 contains conserved B9 domains that mediate interactions with other ciliary proteins. Its recombinant version retains these functional domains, allowing researchers to explore its role in ciliary gatekeeping, membrane protein trafficking, and signaling modulation. Additionally, recombinant B9D1 is utilized in antibody development, drug screening, and diagnostic tools for ciliopathy-related conditions.
Overall, B9D1 recombinant protein serves as a valuable tool for dissecting ciliary biology, understanding disease pathogenesis, and advancing translational research in developmental and genetic disorders.
×
