质子泵和离子通道微调的ATP4A基因调控网络。

Systems and Synthetic Biology Pub Date : 2013-06-01 Epub Date: 2013-01-09 DOI:10.1007/s11693-012-9103-1
Vijai Singh, Indra Mani, Dharmendra Kumar Chaudhary
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引用次数: 8

摘要

ATP4A编码H(+), K(+)- atp酶的α亚基,该亚基含有酶的催化位点,通过细胞膜形成孔,允许离子运输。H(+), K(+)-ATP酶是一种膜结合的p型ATP酶,存在于壁细胞表面,利用ATP水解每个周期产生的能量,帮助离子(H(+), K(+)和Cl(-))在细胞膜上交换,分泌酸进入胃腔。通过同源性建模得到H(+), K(+)- atp酶α-亚基的三维模型。根据自由能和氨基酸残基对其进行了评价和验证。通过分子对接,在三维模型中确定了结合氨基酸活性袋的抑制剂。奥美拉唑和雷贝拉唑与H(+)、K(+)- atp酶α-亚基生成的药物-蛋白相互作用亲和力模型相互作用更强。我们已经建立了ATP4A基因与其他蛋白相互作用的调控网络,这些蛋白参与调控可以帮助质子泵和离子通道的微调。这些发现为发现和开发质子泵抑制剂和ATPase基因调控提供了新的视角。这有助于更好地理解人体生理学,也有助于利用合成生物学策略对胃溃疡的壁细胞进行重编程控制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
ATP4A gene regulatory network for fine-tuning of proton pump and ion channels.

The ATP4A encodes α subunit of H(+), K(+)-ATPase that contains catalytic sites of the enzyme forming pores through cell membrane which allows the ion transport. H(+), K(+)-ATPase is a membrane bound P-type ATPase enzyme which is found on the surface of parietal cells and uses the energy derived from each cycle of ATP hydrolysis that can help in exchanging ions (H(+), K(+) and Cl(-)) across the cell membrane secreting acid into the gastric lumen. The 3-D model of α-subunit of H(+), K(+)-ATPase was generated by homology modeling. It was evaluated and validated on the basis of free energies and amino acid residues. The inhibitor binding amino acid active pockets were identified in the 3-D model by molecular docking. The two drugs Omeprazole and Rabeprazole were found more potent interactions with generated model of α-subunit of H(+), K(+)-ATPase on the basis of their affinity between drug-protein interactions. We have generated ATP4A gene regulatory networks for interactions with other proteins which involved in regulation that can help in fine-tuning of proton pump and ion channels. These findings provide a new dimension for discovery and development of proton pump inhibitors and gene regulation of the ATPase. It can be helpful in better understanding of human physiology and also using synthetic biology strategy for reprogramming of parietal cells for control of gastric ulcers.

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