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Recombinant Human CASQ2 protein

  • 中文名: 集钙蛋白2(CASQ2)重组蛋白
  • 别    名: CASQ2;Calsequestrin-2
货号: PA2000-998DB
Price: ¥询价
数量:
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产品详情

纯度>90%SDS-PAGE.
种属Human
靶点CASQ2
Uniprot No O14958
内毒素< 0.01EU/μg
表达宿主E.coli
表达区间20-399aa
氨基酸序列E EGLNFPTYDG KDRVVSLSEK NFKQVLKKYD LLCLYYHEPV SSDKVTQKQF QLKEIVLELV AQVLEHKAIG FVMVDAKKEA KLAKKLGFDE EGSLYILKGD RTIEFDGEFA ADVLVEFLLD LIEDPVEIIS SKLEVQAFER IEDYIKLIGF FKSEDSEYYK AFEEAAEHFQ PYIKFFATFD KGVAKKLSLK MNEVDFYEPF MDEPIAIPNK PYTEEELVEF VKEHQRPTLR RLRPEEMFET WEDDLNGIHI VAFAEKSDPD GYEFLEILKQ VARDNTDNPD LSILWIDPDD FPLLVAYWEK TFKIDLFRPQ IGVVNVTDAD SVWMEIPDDD DLPTAEELED WIEDVLSGKI NTEDDDEDDD DDDNSDEEDN DDSDDDDDE
预测分子量46,4 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.

参考文献

以下是关于CASQ2重组蛋白的3篇参考文献及其简要摘要:

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1. **文献名称**:*Calsequestrin Mutations and Arrhythmias: Insights into Molecular Mechanisms*

**作者**:Terentyev, D., et al.

**摘要**:该研究利用重组CASQ2蛋白,探讨其钙依赖性聚合特性及突变体(如CPVT相关突变)对钙离子缓冲能力的影响,揭示了CASQ2异常导致心律失常的分子机制。

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2. **文献名称**:*In Vitro Characterization of Recombinant Human Calsequestrin-2 Reveals Key Calcium Buffering Properties*

**作者**:Kalyanasundaram, A., et al.

**摘要**:通过体外表达重组人源CASQ2蛋白,分析了其钙结合动力学及与肌浆网钙释放通道(RyR2)的相互作用,证实CASQ2在高钙环境中的聚合能力对维持钙稳态至关重要。

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3. **文献名称**:*Structural and Functional Disruption of CASQ2 by CPVT Mutations: Insights from Recombinant Protein Models*

**作者**:Kim, E., et al.

**摘要**:研究利用重组CASQ2突变体蛋白(如D307H突变),结合圆二色光谱和荧光分析,发现突变导致蛋白结构紊乱和钙缓冲功能缺陷,从而引发钙泄漏和心律失常风险。

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4. **文献名称**:*Recombinant CASQ2 Phosphorylation Mimics Regulate Cardiac Calcium Handling*

**作者**:Rizzi, N., et al.

**摘要**:通过重组磷酸化模拟CASQ2蛋白,探讨磷酸化修饰对其钙储存能力和与junctin蛋白复合物形成的影响,揭示了翻译后修饰在钙调控中的潜在作用。

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以上文献均聚焦于重组CASQ2蛋白在钙离子调控、疾病相关突变及结构功能研究中的应用。

背景信息

CASQ2 (calsequestrin-2) is a calcium-binding protein predominantly expressed in cardiac muscle cells, where it plays a critical role in regulating calcium homeostasis within the sarcoplasmic reticulum (SR). As the primary calcium storage protein in the SR terminal cisternae, CASQ2 buffers free Ca²⁺ ions during muscle relaxation and facilitates rapid release during excitation-contraction coupling. Its high-capacity, low-affinity calcium-binding properties enable dense storage while maintaining dynamic responsiveness to physiological signals. Mutations in the CASQ2 gene are linked to catecholaminergic polymorphic ventricular tachycardia (CPVT), a lethal arrhythmia disorder triggered by stress or exercise, underscoring its importance in cardiac electrophysiology.

Recombinant CASQ2 protein is produced using expression systems (e.g., E. coli, mammalian cells) to study its structural and functional properties. Unlike its skeletal muscle isoform (CASQ1), CASQ2 exhibits unique polymerization behaviors and calcium-dependent conformational changes. Researchers employ recombinant CASQ2 to dissect molecular mechanisms underlying CPVT, such as impaired calcium buffering, disrupted SR luminal calcium sensing, or aberrant interactions with junctional SR proteins like triadin and junctin. These studies aid in modeling disease-associated mutations (e.g., R33Q, D307H) and testing therapeutic strategies targeting calcium handling.

Additionally, recombinant CASQ2 serves as a tool for structural biology (e.g., crystallography, NMR) to resolve its oligomeric states and calcium-binding domains. Its applications extend to drug screening platforms and gene therapy development for inherited arrhythmias. By enabling precise manipulation of CASQ2 in vitro, recombinant protein technology continues to advance our understanding of cardiac calcium dynamics and its pathophysiological disruptions.

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