| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | KCNJ5 |
| Uniprot No | P48544 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-419aa |
| 氨基酸序列 | MAGDSRNAMNQDMEIGVTPWDPKKIPKQARDYVPIATDRTRLLAEGKKPRQRYMEKSGKCNVHHGNVQETYRYLSDLFTTLVDLKWRFNLLVFTMVYTVTWLFFGFIWWLIAYIRGDLDHVGDQEWIPCVENLSGFVSAFLFSIETETTIGYGFRVITEKCPEGIILLLVQAILGSIVNAFMVGCMFVKISQPKKRAETLMFSNNAVISMRDEKLCLMFRVGDLRNSHIVEASIRAKLIKSRQTKEGEFIPLNQTDINVGFDTGDDRLFLVSPLIISHEINQKSPFWEMSQAQLHQEEFEVVVILEGMVEATGMTCQARSSYMDTEVLWGHRFTPVLTLEKGFYEVDYNTFHDTYETNTPSCCAKELAEMKREGRLLQYLPSPPLLGGCAEAGLDAEAEQNEEDEPKGLGGSREARGSV |
| 预测分子量 | 47,6 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篇关于KCNJ5重组蛋白的关键文献摘要：
1. **文献名称**：*"KCNJ5 Mutations in Aldosterone-Producing Adenomas and Hereditary Hypertension"*
**作者**：Choi M. et al. (2013)
**摘要**：研究发现肾上腺醛固酮瘤中KCNJ5基因的体细胞突变(如G151R、L168R)导致重组蛋白的离子选择性改变，引发钠泄漏和细胞去极化，从而驱动醛固酮过度分泌。
2. **文献名称**：*"Somatic Mutations in ATP1A1 and KCNJ5 Determine the Constitutive Activation of Aldosterone Synthase"*
**作者**：Scholl U.I. et al. (2015)
**摘要**：通过体外重组蛋白实验，证实KCNJ5突变(如T158A)破坏Kir3.4通道的门控机制，导致肾上腺细胞异常去极化和钙信号激活，促进醛固酮合成。
3. **文献名称**：*"Novel Somatic Mutations in KCNJ5 in Primary Aldosteronism"*
**作者**：Monticone S. et al. (2012)
**摘要**：研究利用重组KCNJ5蛋白模型，揭示体细胞突变(如G151E)通过改变通道对钠离子的通透性，持续激活肾上腺皮质细胞的醛固酮分泌通路。
4. **文献名称**：*"Pathological Role of Potassium Channel Mutations in Adrenal Aldosterone-Producing Adenomas"*
**作者**：Tucker S.J. et al. (2013)
**摘要**：通过电生理学分析重组KCNJ5突变体，发现部分突变(如L168R)破坏Kir3.4通道的pH敏感性，导致持续开放状态和醛固酮异常分泌。
这些研究均通过重组蛋白技术解析KCNJ5突变对离子通道功能的影响，并关联其在肾上腺疾病中的病理机制。
**Background of KCNJ5 Recombinant Protein**
KCNJ5. also known as potassium inwardly rectifying channel subfamily J member 5 or Kir3.4. is a gene encoding a protein subunit of G protein-gated inwardly rectifying potassium (GIRK) channels. These channels regulate cellular excitability by mediating potassium ion flow across cell membranes, contributing to membrane repolarization and resting potential maintenance. KCNJ5 forms heterotetrameric channels, often assembling with other Kir3 subunits (e.g., Kir3.1), and is activated via G protein-coupled receptors (GPCRs) linked to neurotransmitters or hormones.
KCNJ5 is highly expressed in the adrenal glands, heart, and brain. Its dysfunction is linked to human diseases, notably primary aldosteronism (PA), a hormone disorder causing hypertension. Somatic or germline mutations in KCNJ5. such as p.Gly151Arg or p.Leu168Arg, alter channel selectivity, leading to sodium influx, adrenal cell depolarization, and excessive aldosterone production. These mutations are found in ~40% of aldosterone-producing adenomas. Additionally, KCNJ5 variants are associated with cardiac arrhythmias, underscoring its role in heart electrophysiology.
Recombinant KCNJ5 protein is engineered for functional and structural studies. Produced in heterologous systems (e.g., mammalian cells, Escherichia coli), it enables researchers to investigate mutation effects, channel pharmacology, and interactions with regulatory proteins. Its applications include drug screening for PA and arrhythmia therapies, as well as structural analyses (e.g., cryo-EM) to elucidate gating mechanisms. Recombinant KCNJ5 thus serves as a critical tool for understanding potassium channel biology and developing targeted treatments for channelopathies.
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