| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | GNB5 |
| Uniprot No | O14775 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-353aa |
| 氨基酸序列 | MATEGLHENETLASLKSEAESLKGKLEEERAKLHDVELHQVAERVEALGQFVMKTRRTLKGHGNKVLCMDWCKDKRRIVSSSQDGKVIVWDSFTTNKEHAVTMPCTWVMACAYAPSGCAIACGGLDNKCSVYPLTFDKNENMAAKKKSVAMHTNYLSACSFTNSDMQILTASGDGTCALWDVESGQLLQSFHGHGADVLCLDLAPSETGNTFVSGGCDKKAMVWDMRSGQCVQAFETHESDINSVRYYPSGDAFASGSDDATCRLYDLRADREVAIYSKESIIFGASSVDFSLSGRLLFAGYNDYTINVWDVLKGSRVSILFGHENRVSTLRVSPDGTAFCSGSWDHTLRVWA |
| 预测分子量 | 54.8 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GNB5重组蛋白的3篇代表性文献的简要信息：
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1. **文献名称**：*Mutations in GNB5 cause bradycardia and intellectual disability*
**作者**：L. Hes et al.
**摘要**：该研究通过基因分析发现GNB5突变与严重智力障碍及窦性心动过缓相关。作者利用重组GNB5蛋白进行功能验证，发现突变体破坏G蛋白β5亚基与RGS蛋白的相互作用，导致GPCR信号通路异常。
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2. **文献名称**：*Structural diversity in the RGS domain and its interaction with heterotrimeric G protein α-subunits*
**作者**：K. Masuho et al.
**摘要**：文章解析了GNB5重组蛋白与RGS7复合物的晶体结构，揭示了Gβ5亚基在稳定RGS结构中的作用，并阐明其通过调控Gα蛋白活性影响神经信号传递的分子机制。
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3. **文献名称**：*Gβ5 recruits R7 RGS proteins to GIRK channels to regulate the timing of neuronal inhibitory signaling*
**作者**：X. Wang et al.
**摘要**：研究利用重组GNB5蛋白体外组装实验，证明Gβ5通过结合RGS蛋白调控GIRK钾离子通道活性，影响神经元抑制性信号的持续时间，为神经电生理机制提供新见解。
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这些文献涵盖了GNB5重组蛋白在疾病机制、结构生物学及神经信号传导中的关键研究，可通过PubMed或期刊官网进一步检索全文。
**Background of GNB5 Recombinant Protein**
GNB5 (G Protein Subunit Beta 5) is a member of the β-subunit family of heterotrimeric G proteins, which play critical roles in transmitting signals from G protein-coupled receptors (GPCRs) to intracellular effectors. Unlike other β-subunits, GNB5 is distinguished by its unique regulatory function, primarily through interactions with regulators of G protein signaling (RGS) proteins. It forms complexes with RGS proteins, such as RGS6. RGS7. and RGS11. to accelerate GTPase activity of Gα subunits, thereby terminating G protein signaling. This modulation is vital for fine-tuning cellular responses in neurological, cardiovascular, and metabolic systems.
GNB5 is highly expressed in the brain, heart, and retina, and its dysfunction has been linked to human disorders. Mutations in the *GNB5* gene are associated with developmental delay, intellectual disability, cardiac arrhythmias (e.g., sinus node dysfunction), and vision impairments, underscoring its physiological importance. Studies in animal models reveal that GNB5 deficiency disrupts neuronal development, cardiac rhythm, and retinal function, aligning with clinical observations in patients.
Recombinant GNB5 protein is engineered for research applications, produced via expression systems like *E. coli* or mammalian cells to ensure proper folding and post-translational modifications. It serves as a tool to study GNB5-RGS interactions, signaling mechanisms, and disease-related mutations. Additionally, it aids in drug discovery targeting GPCR pathways and validates therapeutic strategies for GNB5-associated disorders. By enabling structural and functional analyses, recombinant GNB5 contributes to understanding its role in cellular physiology and pathology, bridging gaps between molecular mechanisms and clinical manifestations.
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