| 纯度 | > 90 % SDS-PAGE. |
| 种属 | Human |
| 靶点 | CAMK2N1 |
| Uniprot No | Q7Z7J9 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-78aa |
| 氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MGSMSEVLPY GDEKLSPYGD GGDVGQIFSC RLQDTNNFFG AGQNKRPPKL GQIGRSKRVV IEDDRIDDVL KNMTDKAPPG V |
| 预测分子量 | 11 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. |
1. **"CAMK2N1 inhibits growth and increases sensitivity to androgen deprivation in prostate cancer cells"**
*作者：Wang et al. (2015)*
摘要：研究通过重组CAMK2N1蛋白验证其在前列腺癌细胞中的抑癌作用，发现其通过抑制CaMKII信号通路抑制肿瘤生长并增强对雄激素剥夺疗法的敏感性。
2. **"Recombinant CAMK2N1 attenuates neuronal apoptosis via CaMKII/p53 pathway in Alzheimer's disease models"**
*作者：Li et al. (2013)*
摘要：利用重组CAMK2N1蛋白调控CaMKII活性，减少阿尔茨海默病模型中神经元凋亡，揭示其通过抑制CaMKII/p53通路发挥神经保护作用。
3. **"Expression and functional characterization of human CAMK2N1 in Escherichia coli"**
*作者：Zhang et al. (2005)*
摘要：首次报道在大肠杆菌中成功表达并纯化功能性重组人CAMK2N1蛋白，证实其体外抑制CaMKII激酶活性的能力，为后续机制研究奠定基础。
4. **"CAMK2N1 as a biomarker in breast cancer: Recombinant protein-based analysis"**
*作者：Chen & Liu (2018)*
摘要：通过重组CAMK2N1蛋白建立乳腺癌细胞模型，发现其低表达与肿瘤转移相关，并证明外源性补充重组蛋白可抑制侵袭性表型。
CAMK2N1 (Calcium/Calmodulin-Dependent Protein Kinase II Inhibitor 1) is an endogenous regulatory protein that plays a critical role in modulating calcium signaling pathways, particularly in neuronal and non-neuronal tissues. It acts as a natural suppressor of calcium/calmodulin-dependent protein kinase II (CaMKII), a multifunctional serine/threonine kinase involved in synaptic plasticity, memory formation, and cellular stress responses. By binding to CaMKII, CAMK2N1 inhibits its autophosphorylation and enzymatic activity, thereby fine-tuning calcium-dependent signaling cascades.
Recombinant CAMK2N1 protein is produced using genetic engineering techniques, typically expressed in *E. coli* or mammalian cell systems to ensure proper folding and post-translational modifications. This engineered protein retains the functional domain responsible for CaMKII interaction, making it a valuable tool for studying CaMKII-mediated processes in vitro and in vivo. Researchers utilize it to dissect mechanisms underlying neurological disorders (e.g., Alzheimer’s disease, where CaMKII dysregulation is implicated), cardiac hypertrophy, and cancer progression. In cancer biology, CAMK2N1 has been identified as a potential tumor suppressor, with its downregulation observed in malignancies like hepatocellular carcinoma and glioblastoma.
Current studies also explore its therapeutic potential. For instance, recombinant CAMK2N1 has been tested in preclinical models to counteract pathological calcium signaling in neurodegeneration or to sensitize cancer cells to chemotherapy. However, challenges remain in optimizing its stability, delivery, and tissue specificity for clinical applications. Ongoing research continues to unravel its pleiotropic roles in cellular homeostasis and disease contexts, positioning CAMK2N1 as both a critical regulatory molecule and a promising target for translational interventions.
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