| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | PDE3A |
| Uniprot No | Q14432 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 669-1141aa |
| 氨基酸序列 | KPILAPEPLVMDNLDSIMEQLNTWNFPIFDLVENIGRKCGRILSQVSYRL FEDMGLFEAFKIPIREFMNYFHALEIGYRDIPYHNRIHATDVLHAVWYLT TQPIPGLSTVINDHGSTSDSDSDSGFTHGHMGYVFSKTYNVTDDKYGCLS GNIPALELMALYVAAAMHDYDHPGRTNAFLVATSAPQAVLYNDRSVLENH HAAAAWNLFMSRPEYNFLINLDHVEFKHFRFLVIEAILATDLKKHFDFVA KFNGKVNDDVGIDWTNENDRLLVCQMCIKLADINGPAKCKELHLQWTDGI VNEFYEQGDEEASLGLPISPFMDRSAPQLANLQESFISHIVGPLCNSYDS AGLMPGKWVEDSDESGDTDDPEEEEEEAPAPNEEETCENNESPKKKTFKR RKIYCQITQHLLQNHKMWKKVIEEEQRLAGIENQSLDQTPQSHSSEQIQA IKEEEEEKGKPRGEEIPTQKPDQ |
| 预测分子量 | 82 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3篇与PDE3A重组蛋白相关的文献示例及其摘要概括：
1. **"Characterization of recombinant human PDE3A expressed in Sf9 insect cells"**
*Authors: Shakur Y, Holst LS, Landstrom TR, et al.*
摘要：该研究利用杆状病毒系统在Sf9昆虫细胞中重组表达人源PDE3A，并系统分析了其酶动力学特性及环核苷酸底物特异性，揭示了其与心血管功能调控的关联。
2. **"Structural insights into PDE3A substrate specificity and inhibition mechanisms"**
*Authors: Zhang Y, Wang L, Hebert TE, et al.*
摘要：通过X射线晶体学解析重组PDE3A蛋白的催化结构域三维结构，阐明了其与选择性抑制剂(如cilostamide)的结合模式，为靶向药物设计提供了结构基础。
3. **"Recombinant PDE3A regulates cardiomyocyte cAMP signaling and contractility"**
*Authors: Movsesian MA, Ahmad F, Hirsch E*
摘要：研究证明重组PDE3A蛋白通过调控心肌细胞cAMP水平影响钙离子动态及收缩功能，揭示了其在心力衰竭病理中的潜在作用靶点。
4. **"PDE3A suppression via recombinant protein delivery inhibits cancer cell proliferation"**
*Authors: Takahashi R, Jiang X, Kokubu Y, et al.*
摘要：利用重组PDE3A蛋白递送系统干预肿瘤细胞，发现其通过调节cAMP/PKA信号通路抑制癌细胞增殖，提示其作为肿瘤治疗新策略的可能性。
(注：上述文献标题及作者为示例性虚构，实际研究需通过PubMed/Google Scholar检索确认。)
**Background of PDE3A Recombinant Protein**
Phosphodiesterase 3A (PDE3A) is a member of the phosphodiesterase enzyme family, which hydrolyzes cyclic nucleotides (cAMP and cGMP) to regulate intracellular signaling pathways. PDE3A specifically modulates cAMP degradation, playing a critical role in cardiovascular function, lipid metabolism, platelet aggregation, and smooth muscle contraction. It is encoded by the *PDE3A* gene located on chromosome 12 in humans and is highly expressed in tissues such as the heart, vascular smooth muscle, and adipose tissue. Dysregulation of PDE3A activity has been implicated in pathologies like hypertension, heart failure, insulin resistance, and thrombotic disorders, making it a therapeutic target for drug development.
Recombinant PDE3A protein is engineered through molecular cloning and expression systems (e.g., *E. coli*, mammalian cells) to produce purified, functional enzyme for research and therapeutic applications. The recombinant form typically retains key structural domains, including the catalytic domain responsible for cyclic nucleotide hydrolysis and regulatory regions that influence enzyme activity. Researchers utilize this protein to study PDE3A’s enzymatic kinetics, substrate specificity, and interactions with inhibitors (e.g., cilostazol, milrinone) in vitro.
In drug discovery, PDE3A recombinant protein serves as a tool for high-throughput screening of potential inhibitors to treat cardiovascular diseases or metabolic syndromes. It also aids in structural studies (e.g., X-ray crystallography) to elucidate mechanisms of enzyme activation or inhibition. Additionally, PDE3A variants linked to genetic disorders, such as hypertension syndromes, are analyzed using recombinant proteins to dissect mutation-driven functional alterations.
Overall, PDE3A recombinant protein bridges basic research and clinical translation, offering insights into cAMP-mediated signaling and paving the way for novel therapeutics targeting PDE3A-associated diseases.
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