纯度 | >85%SDS-PAGE. |
种属 | Human |
靶点 | PRKG2 |
Uniprot No | Q13237 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 2-762aa |
氨基酸序列 | GNGSVKPKH SKHPDGHSGN LTTDALRNKV TELERELRRK DAEIQEREYH LKELREQLSK QTVAIAELTE ELQNKCIQLN KLQDVVHMQG GSPLQASPDK VPLEVHRKTS GLVSLHSRRG AKAGVSAEPT TRTYDLNKPP EFSFEKARVR KDSSEKKLIT DALNKNQFLK RLDPQQIKDM VECMYGRNYQ QGSYIIKQGE PGNHIFVLAE GRLEVFQGEK LLSSIPMWTT FGELAILYNC TRTASVKAIT NVKTWALDRE VFQNIMRRTA QARDEQYRNF LRSVSLLKNL PEDKLTKIID CLEVEYYDKG DYIIREGEEG STFFILAKGK VKVTQSTEGH DQPQLIKTLQ KGEYFGEKAL ISDDVRSANI IAEENDVACL VIDRETFNQT VGTFEELQKY LEGYVANLNR DDEKRHAKRS MSNWKLSKAL SLEMIQLKEK VARFSSSSPF QNLEIIATLG VGGFGRVELV KVKNENVAFA MKCIRKKHIV DTKQQEHVYS EKRILEELCS PFIVKLYRTF KDNKYVYMLL EACLGGELWS ILRDRGSFDE PTSKFCVACV TEAFDYLHRL GIIYRDLKPE NLILDAEGYL KLVDFGFAKK IGSGQKTWTF CGTPEYVAPE VILNKGHDFS VDFWSLGILV YELLTGNPPF SGVDQMMTYN LILKGIEKMD FPRKITRRPE DLIRRLCRQN PTERLGNLKN GINDIKKHRW LNGFNWEGLK ARSLPSPLQR ELKGPIDHSY FDKYPPEKGM PPDELSGWDK DF |
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PRKG2重组蛋白的3篇示例参考文献(注:以下为模拟内容,实际文献请通过学术数据库检索):
1. **文献名称**:*Structural and functional analysis of recombinant PRKG2 in cartilage development*
**作者**:Smith A, et al.
**摘要**:本研究通过重组表达人源PRKG2蛋白,解析其晶体结构,并证明其在调控软骨细胞分化和骨骼生长板信号通路中的关键作用。
2. **文献名称**:*PRKG2 recombinant protein suppresses colorectal cancer progression via cGMP-PKG signaling*
**作者**:Zhang L, et al.
**摘要**:利用重组PRKG2蛋白处理结肠癌细胞,发现其通过激活cGMP-PKG通路抑制肿瘤细胞增殖和迁移,提示其作为潜在肿瘤治疗靶点。
3. **文献名称**:*Recombinant PRKG2 rescues intestinal dysfunction in a mouse knockout model*
**作者**:Tanaka K, et al.
**摘要**:在PRKG2基因敲除小鼠模型中,外源性重组PRKG2蛋白恢复了肠道平滑肌收缩功能,证实其在维持胃肠道运动中的生理必要性。
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**备注**:以上为基于PRKG2已知功能的模拟文献,真实文献可通过PubMed/Google Scholar以关键词"PRKG2 recombinant protein"或"PRKG2 signaling"检索。实际研究中建议优先选择近五年内发表的论文。
**Background of PRKG2 Recombinant Protein**
PRKG2 (cGMP-dependent protein kinase II) is a serine/threonine kinase that acts as a key mediator of intracellular cGMP signaling. Encoded by the *PRKG2* gene in humans, this enzyme is primarily expressed in tissues such as bone, brain, and intestinal epithelium. It plays a critical role in regulating diverse physiological processes, including skeletal development, cell proliferation, and ion transport. PRKG2 is activated by cyclic guanosine monophosphate (cGMP), which induces conformational changes to expose its catalytic domain, enabling phosphorylation of downstream targets.
Structurally, PRKG2 contains an N-terminal regulatory domain with tandem cGMP-binding motifs and a C-terminal catalytic domain. Unlike its isoform PRKG1. PRKG2 lacks a transmembrane domain but includes a unique leucine zipper motif facilitating dimerization. Dysregulation of PRKG2 has been implicated in pathological conditions, such as osteochondrodysplasias, cardiovascular disorders, and gastrointestinal cancers, highlighting its therapeutic relevance.
Recombinant PRKG2 protein is engineered using expression systems (e.g., *E. coli* or mammalian cells*) to produce purified, bioactive kinase for research and drug discovery. Its recombinant form enables studies on cGMP signaling mechanisms, kinase-substrate interactions, and high-throughput screening of modulators. Additionally, it serves as a tool to investigate PRKG2's role in diseases and evaluate its potential as a therapeutic target or biomarker.
The development of PRKG2 recombinant protein has advanced our understanding of cGMP-dependent pathways and accelerated translational research in bone disorders, neurodegeneration, and cancer biology.
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