| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | RhoC |
| Uniprot No | P08134 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-190aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMAAIRKKLVIVGDGACGKTCLLIVFSKDQF PEVYVPTVFENYIADIEVDGKQVELALWDTAGQEDYDRLRPLSYPDTDVI LMCFSIDSPDSLENIPEKWTPEVKHFCPNVPIILVGNKKDLRQDEHTRRE LAKMKQEPVRSEEGRDMANRISAFGYLECSAKTKEGVREVFEMATRAGLQ VRKNKRRRGC |
| 预测分子量 | 24 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RhoC重组蛋白的3-4篇参考文献的示例(注：以下为模拟文献，实际引用时请核实真实来源)：
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1. **文献名称**：*"RhoC GTPase regulates tumor invasion through cytoskeletal reorganization in recombinant protein models"*
**作者**：Li, J. et al.
**摘要**：研究利用重组RhoC蛋白处理多种癌细胞系，发现其通过激活ROCK信号通路促进肌动蛋白骨架重排，增强癌细胞迁移和侵袭能力，提示RhoC在肿瘤转移中的关键作用。
2. **文献名称**：*"Expression and functional analysis of recombinant RhoC in hepatocellular carcinoma metastasis"*
**作者**：Zhang, Y. et al.
**摘要**：通过构建重组RhoC蛋白，验证其在肝癌细胞中过表达可诱导上皮-间质转化(EMT)，并增加细胞外基质降解酶MMP-9的分泌，从而促进肝内转移。
3. **文献名称**：*"Recombinant RhoC protein enhances endothelial cell permeability via ERK signaling pathway"*
**作者**：Kim, S. et al.
**摘要**：实验表明，重组RhoC蛋白通过激活ERK磷酸化，破坏血管内皮细胞间连接蛋白(如VE-cadherin)，导致血管通透性升高，可能解释肿瘤血管渗漏的机制。
4. **文献名称**：*"In vitro characterization of RhoC recombinant protein in fibroblast-mediated matrix remodeling"*
**作者**：Garcia, R. et al.
**摘要**：研究发现重组RhoC蛋白可诱导成纤维细胞收缩及胶原纤维重组，为肿瘤微环境中基质硬化及促转移机制提供了体外模型支持。
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如需真实文献，建议在PubMed或Web of Science中检索关键词“RhoC recombinant protein”或“RhoC overexpression”，并筛选近年高被引研究。
RhoC (Ras homolog family member C) is a small GTPase belonging to the Rho subfamily of the Ras superfamily, widely recognized for its critical role in regulating cytoskeletal dynamics, cell motility, and intracellular signaling pathways. Discovered in the 1990s, RhoC shares ~90% amino acid sequence identity with RhoA but exhibits distinct functional characteristics, particularly in promoting invasive cell behavior. It functions as a molecular switch, cycling between active GTP-bound and inactive GDP-bound states, mediated by guanine nucleotide exchange factors (GEFs), GTPase-activating proteins (GAPs), and guanine nucleotide dissociation inhibitors (GDIs).
Research has highlighted RhoC's overexpression in aggressive cancers, including breast, pancreatic, prostate, and ovarian cancers, where it drives metastasis by enhancing cell migration, invasion, and survival under stress conditions. Its dysregulation is linked to epithelial-mesenchymal transition (EMT), angiogenesis, and resistance to chemotherapy. Unlike RhoA, RhoC localizes to both the cytoplasm and membrane, enabling unique interactions with downstream effectors like ROCK, mDia, and PAK to modulate actin polymerization, focal adhesion assembly, and matrix remodeling.
Recombinant RhoC proteins are engineered using expression systems (e.g., E. coli, mammalian cells) to produce purified, functional RhoC for mechanistic studies. These proteins retain post-translational modifications (e.g., prenylation) critical for membrane association and activity. Applications include in vitro GTPase activity assays, screening for RhoC-targeted inhibitors, and studying metastasis-related signaling crosstalk. Recent efforts explore therapeutic strategies to inhibit RhoC or its pathways, leveraging recombinant tools to validate drug candidates and decode its role in tumor microenvironments. Despite progress, challenges remain in understanding context-dependent RhoC regulation and developing selective inhibitors without disrupting related GTPases.
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