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敲除 insrr 基因的小鼠对实验性碱中毒的反应不足。

Deficient Response to Experimentally Induced Alkalosis in Mice with the Inactivated insrr Gene.

机构信息

Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences.

出版信息

Acta Naturae. 2011 Oct;3(4):114-7.

PMID:22649711
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3347619/
Abstract

Currently, the molecular mechanisms of the acid-base equilibrium maintenance in the body remain poorly understood. The development of alkalosis under various pathological conditions poses an immediate threat to human life. Understanding the physiological mechanisms of alkalosis compensation may stimulate the development of new therapeutic approaches and new drugs for treatment. It was previously shown that the orphan insulin receptor-related receptor (IRR) is activated by mildly alkaline media. In this study, we analyzed mutant mice with targeted inactivation of theinsrr gene encoding IRR, and revealed their phenotype related to disorders of the acid-base equilibrium. Higher concentrations of bicarbonate and CO(2)were found in the blood ofinsrr knockout mice in response to metabolic alkalosis.

摘要

目前,机体酸碱平衡维持的分子机制仍知之甚少。在各种病理条件下碱中毒的发生对人类生命构成直接威胁。了解碱中毒代偿的生理机制可能会刺激新的治疗方法和药物的开发。先前的研究表明,孤儿胰岛素受体相关受体(IRR)可被轻度碱性介质激活。在这项研究中,我们分析了靶向敲除编码 IRR 的 insrr 基因的突变小鼠,并揭示了它们与酸碱平衡紊乱相关的表型。代谢性碱中毒时,insrr 基因敲除小鼠的血液中碳酸氢盐和 CO(2)浓度升高。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efe5/3347619/ef39540a3756/AN20758251-11-114-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efe5/3347619/21de2e8812f0/AN20758251-11-114-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efe5/3347619/ef39540a3756/AN20758251-11-114-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efe5/3347619/21de2e8812f0/AN20758251-11-114-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efe5/3347619/ef39540a3756/AN20758251-11-114-g002.jpg

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本文引用的文献

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Regulation of CIRL-1 proteolysis and trafficking.CIRL-1 蛋白水解和运输的调节。
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