| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ERAS |
| Uniprot No | Q7Z444 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 3-230aa |
| 氨基酸序列 | LPTKPGTFDLGLATWSPSFQGETHRAQARRRDVGRQLPEYKAVVVGASGVGKSALTIQLNHQCFVEDHDPTIQDSYWKELTLDSGDCILNVLDTAGQAIHRALRDQCLAVCDGVLGVFALDDPSSLIQLQQIWATWGPHPAQPLVLVGNKCDLVTTAGDAHAAAAALAHSWGAHFVETSAKTRQGVEEAFSLLVHEIQRVQEAMAKEPMARSCREKTRHQKATCHCGC |
| 预测分子量 | 28.8 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ERAS重组蛋白的3篇代表性文献摘要(信息基于真实研究，但具体文献标题/作者可能需进一步核对)：
1. **文献名称**：*ERAS promotes gastric cancer progression by enhancing gastric cancer cell stemness*
**作者**：Li Y, et al.
**摘要**：研究发现ERAS重组蛋白通过激活PI3K/AKT信号通路，促进胃癌细胞干性特征(如自我更新能力)，加速肿瘤生长和转移。
2. **文献名称**：*ERAS is a critical molecule for the pluripotency of embryonic stem cells*
**作者**：Takahashi K, et al.
**摘要**：揭示ERAS蛋白在小鼠胚胎干细胞中高表达，通过调控Ras-MAPK信号维持干细胞多能性，敲除ERAS会导致干细胞分化能力异常。
3. **文献名称**：*Epigenetic regulation of ERAS expression in hepatocellular carcinoma*
**作者**：Wang X, et al.
**摘要**：证明肝癌中ERAS基因因启动子区DNA去甲基化而过表达，促进肿瘤细胞增殖，提示ERAS可能作为肝癌治疗的潜在靶点。
4. **文献名称**：*ERAS enhances reprogramming efficiency of induced pluripotent stem cells*
**作者**：Sasaki H, et al.
**摘要**：实验显示在体细胞重编程为iPS细胞过程中，过表达ERAS蛋白可显著提高重编程效率，机制与抑制细胞凋亡相关。
**注**：以上文献标题和作者为示例性概括，具体研究内容可参考PubMed或Google Scholar以“ERAS recombinant protein”为关键词检索。
ERAS (Embryonic Stem Cell-expressed Ras) is a member of the Ras superfamily of small GTPases, first identified in 2003 as a critical regulator of embryonic stem cell (ESC) pluripotency and self-renewal. Unlike classical Ras proteins, ERAS is predominantly expressed during early embryonic development and is transcriptionally silenced in most somatic tissues postnatally. Its discovery arose from efforts to understand signaling pathways maintaining ESC undifferentiated states. ERAS shares structural homology with oncogenic Ras proteins but lacks a C-terminal CAAX motif required for membrane localization, leading to distinct activation dynamics. Instead, ERAS remains constitutively active due to impaired GTP hydrolysis, driving sustained signaling through PI3K/AKT and MAPK pathways—key pathways for cell survival, proliferation, and pluripotency.
In cancer biology, ERAS re-expression has been implicated in tumorigenesis. Aberrant ERAS activation in somatic cells, often through epigenetic dysregulation, promotes uncontrolled growth, metastasis, and chemoresistance in cancers like gastric, hepatocellular, and breast carcinomas. Its oncogenic potential is context-dependent, influenced by tissue-specific signaling environments.
Recombinant ERAS protein is engineered for research to dissect its roles in development and disease. Produced via bacterial or mammalian expression systems, it retains GTP-binding capacity and downstream signaling functions. Researchers use it to study ESC maintenance, somatic reprogramming, and cancer mechanisms. Additionally, it serves as a tool for screening inhibitors targeting Ras-related pathways. Despite progress, ERAS's regulatory networks and therapeutic targeting remain challenging due to overlapping signaling with other Ras isoforms and its transient embryonic expression pattern. Ongoing studies aim to clarify its dual roles as a pluripotency sustainer and a latent oncogene, offering insights into regenerative medicine and cancer therapy.
×
