| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | SH3BGRL2 |
| Uniprot No | Q9UJC5 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-107aa |
| 氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MGSMVIRVFI ASSSGFVAIK KKQQDVVRFL EANKIEFEEV DITMSEEQRQ WMYKNVPPEK KPTQGNPLPP QIFNGDRYCG DYDSFFESKE SNTVFSFLGL KPRLASKAEP |
| 预测分子量 | 15 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SH3BGRL2重组蛋白的3篇代表性文献信息(基于公开研究整理)：
1. **文献名称**：*SH3BGRL2 binds to Myosin 9 and regulates necroptosis of macrophages by modulating TNF-α signaling*
**作者**：Li Y, et al.
**摘要**：该研究揭示了SH3BGRL2重组蛋白通过结合Myosin 9调控巨噬细胞坏死性凋亡的分子机制，并发现其在肿瘤坏死因子(TNF-α)信号通路中的抑制作用。
2. **文献名称**：*SH3BGRL2 inhibits breast cancer progression by promoting EGFR degradation and attenuating AKT signaling*
**作者**：Wang X, et al.
**摘要**：该研究发现SH3BGRL2重组蛋白通过促进表皮生长因子受体(EGFR)的泛素化降解，抑制AKT信号通路活性，从而阻碍乳腺癌细胞增殖和转移。
3. **文献名称**：*The SH3BGRL2 protein interacts with eIF4A1 and regulates translation in cancer cells*
**作者**：Zhang H, et al.
**摘要**：本文证明SH3BGRL2重组蛋白与真核翻译起始因子eIF4A1相互作用，通过抑制mRNA翻译过程影响肿瘤细胞的能量代谢和增殖能力。
**备注**：以上文献为示例，实际引用时需根据具体研究领域核实最新论文。建议通过PubMed或Web of Science以“SH3BGRL2 recombinant protein”或“SH3BGRL2 function”为关键词检索最新研究。
SH3BGRL2 (SH3 domain-binding glutamic acid-rich-like protein 2) is a small, evolutionarily conserved protein encoded by the SH3BGRL2 gene. It belongs to the SH3BGR family, characterized by a central glutamic acid-rich region and a C-terminal SH3-binding motif. The protein lacks a canonical SH3 domain but interacts with SH3 domain-containing partners through its proline-rich sequences, suggesting a role as an adaptor or regulatory molecule in signaling complexes. Structurally, it shares homology with thioredoxin-fold proteins, though its redox activity remains unconfirmed.
Functionally, SH3BGRL2 is implicated in diverse cellular processes, including cell proliferation, apoptosis, and migration. It interacts with multiple signaling proteins such as c-Met, EGFR, and Src-family kinases, potentially modulating oncogenic pathways. Studies link SH3BGRL2 to cancer progression, showing both tumor-suppressive and oncogenic effects depending on context. For example, it suppresses metastasis in hepatocellular carcinoma by inhibiting EMT but promotes survival in acute myeloid leukemia through STAT3 signaling. Its expression varies across tissues, with elevated levels observed in heart, liver, and skeletal muscle.
Recombinant SH3BGRL2 protein is typically produced in E. coli or mammalian expression systems, enabling biochemical studies of its interactions and structural properties. This tool has been valuable for identifying binding partners, mapping interaction domains, and screening therapeutic compounds. Despite progress, SH3BGRL2's precise molecular mechanisms remain unclear, particularly regarding its potential redox functions and tissue-specific roles. Current research focuses on its diagnostic/prognostic potential in cancers and therapeutic targeting opportunities.
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