纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | CENTG2 |
Uniprot No | Q9UPQ3 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 1-392aa |
氨基酸序列 | MNYQQQLANSAAIRAEIQRFESVHPNIYSIYELLERVEEPVLQNQIREHVIAIEDAFVNSQEWTLSRSVPELKVGIVGNLASGKSALVHRYLTGTYVQEESPEGGRFKKEIVVDGQSYLLLIRDEGGPPEAQFAMWVDAVIFVFSLEGEISFQTVYHYYSRMANYRNTSEIPLVLVGTQDAISSANPRVIDDARARKLSNDLKRCTYYETCATYGLNVERVFQDVAQKIVATRKKQQLSIGPCKSLPNSPSHSSVCSAQVSAVHISQTSNGGGSLSDYSSSVPSTPSTSQKELRIDVPPTANTPTPVRKQSKRRSNLFTSRKGSDPDKEKKGLESRADSIGSGRAIPIKQGLPFFVLALTASTYLRPAGARARQSSPWPGRAEGWSDQPALC |
分子量 | 69.7 KDa |
蛋白标签 | GST-tag at N-terminal |
缓冲液 | 0 |
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CENTG2(ARAP2)蛋白的几篇代表性文献的简化整理(请注意,以下为模拟示例,实际文献请通过学术数据库确认):
1. **文献名称**:ARAP2 regulates insulin signaling and glucose homeostasis
**作者**:Liu Y, et al.
**摘要**:本研究揭示了ARAP2通过调控Rho GTPases活性参与胰岛素信号通路,重组人ARAP2蛋白体外实验表明其能够结合PI3K产物PIP3.并影响肌动蛋白骨架重组,提示其在代谢疾病中的作用。
2. **文献名称**:Structural analysis of the ARAP2 PH domain bound to phosphoinositides
**作者**:Zhang Q, et al.
**摘要**:利用重组表达的ARAP2蛋白PH结构域进行晶体结构解析,发现其特异性识别PI(3.4.5)P3脂质,为ARAP2在细胞膜定位和信号转导机制提供了结构基础。
3. **文献名称**:ARAP2 modulates cell migration via CDC42 signaling in breast cancer
**作者**:Chen H, et al.
**摘要**:通过重组ARAP2蛋白功能缺失实验,证明其通过调控CDC42 GTPase活性抑制乳腺癌细胞迁移和侵袭,提示其作为肿瘤抑制因子的潜在角色。
4. **文献名称**:ARAP2 interaction with clathrin adaptor proteins in endocytic trafficking
**作者**:Wang L, et al.
**摘要**:利用重组ARAP2蛋白共沉淀技术发现其与AP2复合物相互作用,揭示了ARAP2参与网格蛋白介导的内吞运输,影响受体降解和信号传导。
**建议**:使用PubMed或Google Scholar以“ARAP2 recombinant protein”“CENTG2 function”等关键词检索近5年文献,关注该蛋白在细胞信号、癌症或代谢中的机制研究。
CENTG2. also known as AGAP2 or PIKE (phosphoinositide 3-kinase enhancer), is a member of the ARF GTPase-activating protein (GAP) family. It regulates small GTPases of the ADP-ribosylation factor (ARF) family, which are critical for membrane trafficking, cytoskeletal reorganization, and signal transduction. Structurally, CENTG2 contains a pleckstrin homology (PH) domain that binds phosphoinositides and a GAP domain responsible for accelerating GTP hydrolysis in ARFs, modulating their activity.
Functionally, CENTG2 is implicated in cell migration, proliferation, and survival. It interacts with signaling pathways like PI3K/Akt/mTOR, enhancing cell growth and suppressing apoptosis. Overexpression of CENTG2 has been linked to cancer progression, including glioblastoma, prostate, and lung cancers, where it promotes tumor invasiveness and therapy resistance. Additionally, it may contribute to neurological disorders by affecting neuronal development or degeneration.
Its dual role as a signaling hub and ARF regulator makes CENTG2 a potential therapeutic target. However, its context-dependent mechanisms in disease remain under active investigation.
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