| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CAMK2B |
| Uniprot No | Q13554 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-666aa |
| 氨基酸序列 | MATTVTCTRF TDEYQLYEDI GKGAFSVVRR CVKLCTGHEY AAKIINTKKL SARDHQKLER EARICRLLKH SNIVRLHDSI SEEGFHYLVF DLVTGGELFE DIVAREYYSE ADASHCIQQI LEAVLHCHQM GVVHRDLKPE NLLLASKCKG AAVKLADFGL AIEVQGDQQA WFGFAGTPGY LSPEVLRKEA YGKPVDIWAC GVILYILLVG YPPFWDEDQH KLYQQIKAGA YDFPSPEWDT VTPEAKNLIN QMLTINPAKR ITAHEALKHP WVCQRSTVAS MMHRQETVEC LKKFNARRKL KGAILTTMLA TRNFSVGRQT TAPATMSTAA SGTTMGLVEQ AKSLLNKKAD GVKPQTNSTK NSAAATSPKG TLPPAALEPQ TTVIHNPVDG IKESSDSANT TIEDEDAKAP RVPDILSSVR RGSGAPEAEG PLPCPSPAPF SPLPAPSPRI SDILNSVRRG SGTPEAEGPL SAGPPPCLSP ALLGPLSSPS PRISDILNSV RRGSGTPEAE GPSPVGPPPC PSPTIPGPLP TPSRKQEIIK TTEQLIEAVN NGDFEAYAKI CDPGLTSFEP EALGNLVEGM DFHRFYFENL LAKNSKPIHT TILNPHVHVI GEDAACIAYI RLTQYIDGQG RPRTSQSEET RVWHRRDGKW QNVHFHCSGA PVAPLQ |
| 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CAMK2B重组蛋白的3篇代表性文献(虚构示例，仅供参考格式)：
1. **文献名称**: *Structural insights into the autoinhibition and activation of CaMKIIB*
**作者**: Hojjatian, A., et al.
**摘要**: 本研究通过冷冻电镜解析了重组人源CAMK2B的全长结构，揭示了其自抑制状态下激酶结构域与调节域的相互作用机制，并探讨了钙调蛋白激活后的构象变化对神经元信号转导的影响。
2. **文献名称**: *Recombinant CaMKIIB regulates synaptic plasticity in hippocampal neurons*
**作者**: Hell, J.W., et al.
**摘要**: 通过在大肠杆菌中表达纯化重组CAMK2B蛋白，证明其在体外可磷酸化突触后密度蛋白(如GluN2B)，并验证了其在长时程增强(LTP)中的关键作用，为突触可塑性研究提供工具。
3. **文献名称**: *Expression optimization and functional characterization of CaMKIIB mutants linked to neurodevelopmental disorders*
**作者**: Kool, M.J., et al.
**摘要**: 通过昆虫细胞系统表达重组CAMK2B突变体，发现某些致病突变(如T236R)导致激酶活性异常增强，提示突变蛋白的异常自激活可能与智力障碍相关神经病理机制有关。
注：以上文献为示例性内容，实际文献需通过PubMed/Google Scholar检索关键词(如"recombinant CAMK2B"、"CaMKIIB purification")获取。建议使用真实数据库查询最新研究。
The calcium/calmodulin-dependent protein kinase II beta (CAMK2B) is a member of the CAMKII family, a class of serine/threonine kinases critical for calcium-mediated signaling in eukaryotic cells. CAMK2B is predominantly expressed in the brain, where it plays a central role in synaptic plasticity, learning, and memory. It functions as a multimeric holoenzyme, with its activation triggered by calcium influx, which promotes binding to calmodulin (CaM), inducing autophosphorylation at Thr287. This modification sustains kinase activity even after calcium levels decline, enabling long-term signaling effects. CAMK2B is essential for long-term potentiation (LTP) and depression (LTD), processes underlying neuronal adaptation and cognitive function.
Recombinant CAMK2B protein is engineered through heterologous expression systems, such as *E. coli* or mammalian cell cultures, to produce highly purified, functional kinase for research. Its recombinant form retains enzymatic activity and structural properties, allowing in vitro studies of phosphorylation mechanisms, substrate interactions, and regulatory pathways. Researchers utilize it to investigate CAMK2B's role in neurodevelopment, synaptic signaling, and diseases like Alzheimer's, autism, and schizophrenia, where dysregulated CAMK2B activity is implicated. Additionally, it serves as a tool for drug discovery, enabling screening of inhibitors or modulators targeting its ATP-binding or regulatory domains. Structural studies using recombinant CAMK2B have clarified its autoinhibitory domain organization and CaM-binding dynamics. By providing a controlled, scalable source of the protein, recombinant CAMK2B accelerates mechanistic insights into calcium-dependent signaling and its pathological disruptions.
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