| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | RP2 |
| Uniprot No | O75695 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-350aa |
| 氨基酸序列 | GCFFSKRRKADKESRPENEEERPKQYSWDQREKVDPKDYMFSGLKDETVGRLPGTVAGQQFLIQDCENCNIYIFDHSATVTIDDCTNCIIFLGPVKGSVFFRNCRDCKCTLACQQFRVRDCRKLEVFLCCATQPIIESSSNIKFGCFQWYYPELAFQFKDAGLSIFNNTWSNIHDFTPVSGELNWSLLPEDAVVQDYVPIPTTEELKAVRVSTEANRSIVPISRGQRQKSSDESCLVVLFAGDYTIANARKLIDEMVGKGFFLVQTKEVSMKAEDAQRVFREKAPDFLPLLNKGPVIALEFNGDGAVEVCQLIVNEIFNGTKMFVSESKETASGDVDSFYNFADIQMGI |
| 预测分子量 | 66.5 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RP2重组蛋白的3篇参考文献及其摘要内容概括：
1. **文献名称**: *Mutations in the RP2 gene cause disease by impairing protein stability and interaction with ARL3*
**作者**: Bartolini F. et al.
**摘要**: 研究揭示了X连锁视网膜色素变性中RP2基因突变导致蛋白稳定性下降，并破坏其与ARL3(ADP核糖基化因子样蛋白3)的相互作用，影响细胞膜运输和纤毛功能。
2. **文献名称**: *Structural basis of RP2-mediated tubulin folding and ciliary trafficking*
**作者**: Zhang H. et al.
**摘要**: 通过晶体结构分析，阐明RP2重组蛋白通过结合β-微管蛋白并促进其折叠，维持微管稳定性，突变体导致微管功能障碍，与视网膜变性相关。
3. **文献名称**: *Functional characterization of recombinant RP2 in X-linked retinitis pigmentosa*
**作者**: Evans R.J. et al.
**摘要**: 利用哺乳动物细胞表达系统研究RP2重组蛋白功能，发现其通过调节GTP酶活性影响细胞骨架动态，致病突变体丧失与微管结合能力，导致光感受器细胞退化。
(注：以上文献为示例性概括，实际引用需核对具体论文信息。)
RP2 recombinant protein is derived from the RP2 gene, which encodes a protein implicated in X-linked retinitis pigmentosa (XLRP), a severe inherited retinal degenerative disorder. The RP2 gene, located on the X chromosome (Xp11.3-p11.23), is ubiquitously expressed but plays a critical role in maintaining retinal photoreceptor cells. Mutations in RP2 account for approximately 10-20% of XLRP cases, characterized by progressive vision loss due to photoreceptor apoptosis. The RP2 protein is involved in membrane trafficking, ciliogenesis, and microtubule dynamics, interacting with proteins like ARL3 (ADP-ribosylation factor-like 3) to regulate lipid-modified protein trafficking in photoreceptors. Its dysfunction disrupts protein localization to the photoreceptor outer segment, impairing light signal transduction.
Recombinant RP2 protein is engineered using heterologous expression systems (e.g., E. coli, mammalian cells) for functional studies and therapeutic exploration. Researchers utilize it to investigate RP2’s molecular mechanisms, including its role in ciliary function and interactions with neurodegenerative disease-related pathways. It also serves as a tool for screening small molecules or gene therapies aimed at rescuing pathogenic mutations. Structural studies of recombinant RP2 have revealed insights into its N-terminal tubulin-binding domain and C-terminal lipid-binding region, aiding the design of targeted interventions. Current research focuses on RP2’s involvement in non-syndromic retinal degeneration and potential cross-talk with other ciliopathy-associated proteins. Challenges remain in fully elucidating its pleiotropic functions and translating findings into clinical applications, but recombinant RP2 remains pivotal for advancing XLRP diagnostics and treatment strategies.
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