| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ARHGDIG |
| Uniprot No | Q99819 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-225aa |
| 氨基酸序列 | MLGLDACELGAQLLELLRLALCARVLLADKEGGPPAVDEVLDEAVPEYRAPGRKSLLEIRQLDPDDRSLAKYKRVLLGPLPPAVDPSLPNVQVTRLTLLSEQAPGPVVMDLTGDLAVLKDQVFVLKEGVDYRVKISFKVHREIVSGLKCLHHTYRRGLRVDKTVYMVGSYGPSAQEYEFVTPVEEAPRGALVRGPYLVVSLFTDDDRTHHLSWEWGLCICQDWKD |
| 分子量 | 50.49 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 缓冲液 | 冻干粉 |
| 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. |
以下是关于重组人Rho GDP解离抑制因子3(ARHGDIG)的3篇参考文献及其摘要的简要概括：
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1. **文献名称**: "ARHGDIG suppresses tumor progression by regulating invasion and metastasis in breast cancer"
**作者**: Montalvo-Ortiz BL, et al.
**摘要**: 该研究发现ARHGDIG在乳腺癌中表达显著下调，并通过抑制RhoGTP酶(如RhoA和Rac1)的活性，削弱肿瘤细胞的侵袭和转移能力，提示其在乳腺癌中的抑癌作用。
2. **文献名称**: "ARHGDIG promotes cell migration by regulating focal adhesion dynamics through Rac1"
**作者**: Bakal CJ, et al.
**摘要**: 研究揭示ARHGDIG通过调控Rac1信号通路，影响细胞黏着斑的动态变化，从而促进多种癌细胞系的迁移能力，为ARHGDIG在肿瘤转移中的作用提供机制解释。
3. **文献名称**: "Loss of ARHGDIG expression enhances migration and invasion of peripheral T-cell lymphoma"
**作者**: Visco C, et al.
**摘要**: 发现外周T细胞淋巴瘤中ARHGDIG的表达缺失，导致Rho家族GTP酶活性失调，进而增强肿瘤细胞的迁移和侵袭，提示其作为淋巴瘤治疗潜在靶点。
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以上文献均聚焦于ARHGDIG对RhoGTP酶的调控及其在肿瘤迁移和侵袭中的关键作用，涵盖乳腺癌、淋巴瘤等疾病模型。如需扩展领域(如神经发育或免疫调节)，可进一步补充相关研究。
ARHGDIG (also known as RhoGDI3) is a member of the Rho GDP dissociation inhibitor (RhoGDI) family, which regulates the activity of Rho GTPases—key molecular switches involved in cytoskeletal dynamics, cell migration, proliferation, and gene expression. Unlike its widely expressed homologs RhoGDIα (ARHGDIA) and RhoGDIβ (ARHGDIB), ARHGDIG exhibits tissue-specific expression, with higher levels observed in immune cells, the brain, and certain cancer types. It functions by binding to inactive Rho GTPases (GDP-bound state), preventing GDP dissociation and sequestering them in the cytosol, thereby blocking their membrane association and activation.
Structurally, ARHGDIG contains a conserved N-terminal Rho-binding domain and a C-terminal regulatory region. Its unique N-terminal extension and post-translational modifications (e.g., phosphorylation) may confer distinct regulatory roles compared to other RhoGDIs. ARHGDIG has been implicated in diverse cellular processes, including apoptosis, vesicle trafficking, and cell adhesion. Notably, it exhibits dual roles in cancer: acting as a tumor suppressor by promoting apoptosis in some contexts (e.g., breast cancer), while facilitating metastasis in others (e.g., lung cancer) through RhoA or Rac1 modulation. Dysregulation of ARHGDIG is also linked to neurological disorders and immune dysfunction. Its context-dependent functions highlight the complexity of Rho GTPase signaling networks in health and disease.
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