| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CRK |
| Uniprot No | P46108 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 2-304aa |
| 氨基酸序列 | AGNFDSEER SSWYWGRLSR QEAVALLQGQ RHGVFLVRDS STSPGDYVLS VSENSRVSHY IINSSGPRPP VPPSPAQPPP GVSPSRLRIG DQEFDSLPAL LEFYKIHYLD TTTLIEPVSR SRQGSGVILR QEEAEYVRAL FDFNGNDEED LPFKKGDILR IRDKPEEQWW NAEDSEGKRG MIPVPYVEKY RPASASVSAL IGGNQEGSHP QPLGGPEPGP YAQPSVNTPL PNLQNGPIYA RVIQKRVPNA YDKTALALEV GELVKVTKIN VSGQWEGECN GKRGHFPFTH VRLLDQQNPD EDFS |
| 预测分子量 | 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CRK重组蛋白的3篇参考文献及其摘要概括：
1. **文献名称**：*CRK adaptor protein signaling in cell migration*
**作者**：Feller, S.M.
**摘要**：该文献综述了CRK蛋白作为衔接分子在细胞迁移中的作用，重点讨论了重组CRK蛋白在Ras-MAPK和细胞骨架重组信号通路中的调控机制，及其与肿瘤转移的关联。
2. **文献名称**：*Structural basis for the interaction between the Crk II adaptor protein and c-Abl kinase*
**作者**：Wu, X., et al.
**摘要**：通过X射线晶体学分析，本研究解析了重组CRK-II蛋白的SH3结构域与c-Abl激酶的复合物结构，揭示了二者相互作用的关键位点，为靶向CRK信号通路的药物设计提供依据。
3. **文献名称**：*CRK重组蛋白在肺癌细胞侵袭中的功能研究*
**作者**：李明等
**摘要**：通过构建CRK重组蛋白表达载体，研究发现其在肺癌细胞中过表达可增强细胞侵袭能力，并激活下游FAK/PI3K通路，提示CRK可能成为肺癌治疗的潜在靶点。
(注：以上文献信息为示例性质，实际引用时请核对具体文献内容及作者信息。)
CRK (CT10 regulator of kinase) proteins are a family of adaptor proteins crucial in intracellular signal transduction, primarily involved in mediating protein-protein interactions during cellular processes such as proliferation, migration, adhesion, and apoptosis. The CRK family includes two major isoforms, CRK-I and CRK-II, derived from alternative splicing of the CRK gene. Structurally, CRK proteins contain Src homology 2 (SH2) and Src homology 3 (SH3) domains, enabling them to link tyrosine-phosphorylated receptors or cytoplasmic kinases (via SH2) to downstream effectors (via SH3). This bridging function allows CRK proteins to regulate pathways like Ras/MAPK, PI3K/Akt, and JNK, influencing cell survival and cytoskeletal dynamics.
Initially identified as the human homolog of the v-CRK oncogene from avian retrovirus CT10. CRK gained attention due to its role in cancer. Dysregulation of CRK signaling is associated with tumor progression, metastasis, and drug resistance. Beyond oncology, CRK proteins are implicated in immune responses, neuronal development, and cardiovascular diseases, highlighting their broad physiological relevance.
Recombinant CRK proteins are engineered using expression systems (e.g., E. coli, mammalian cells) to study their structure-function relationships, binding partners, and mechanistic roles in signaling networks. Purified recombinant CRK serves as a tool for in vitro assays, crystallography, or inhibitor screening, aiding drug discovery. Researchers also utilize CRK mutants (e.g., SH2/SH3 domain deletions) to dissect specific interactions or pathway contributions. Despite progress, challenges remain in understanding context-dependent CRK functions, isoform-specific effects, and therapeutic targeting. Ongoing studies aim to clarify CRK's dual roles as a tumor promoter or suppressor and its potential as a biomarker or therapeutic target in precision medicine.
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