If the Gapdh Gene is Continuously Expressed
Abstract—
The most important property of a living organism is the maintenance of optimal acid–base balance and the ionic composition of the internal environment. The kidneys are one of the main pH-regulating organs in the body. Receptor tyrosine kinase IRR (an insulin receptor-related receptor) is an alkaline pH-sensor. In mice (Mus Musculus) with a knockout of the insrr gene encoding the IRR receptor, bicarbonate secretion is impaired under the conditions of alkaline loading, which indicates the role of the receptor tyrosine kinase IRR in the regulation of acid–base balance in the body. In order to search for proteins functionally associated with the receptor tyrosine kinase IRR, we performed a large-scale sequencing of the mouse kidney transcriptome of wild type and insrr knockout mice kept under normal conditions and under alkaline conditions. As a result, we found a decrease in the gapdh gene expression in the kidneys of insrr knockout mice compared to wild type mice. RNA sequencing data were confirmed by TaqMan real-time PCR and Western blotting. Using the TaqMan real-time PCR method, we revealed a decrease in the level of gapdh expression not only in the kidneys, but also in the liver and brain of insrr knockout mice. Thus, the changes in the gapdh gene expression in the kidneys of insrr knockout mice may indicate a functional relationship between genes and a possible role of GAPDH in previously undescribed molecular mechanisms of regulation of acid–base balance in the body.
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Funding
The work was supported by the Russian Foundation for Basic Research, grants nos. 19-34-90177 and 20-04-00880.
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Translated by E. V. Makeeva
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Gantsova, E.A., Gavrilenkova, A.A., Serova, O.V. et al. Changes in the Expression of the gapdh Gene in the Organs of insrr Knockout Mice. Dokl Biol Sci 505, 113–118 (2022). https://doi.org/10.1134/S0012496622040056
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DOI : https://doi.org/10.1134/S0012496622040056
Keywords:
- gapdh
- IRR
- receptor tyrosine kinases
- glyceraldehyde-3-phosphate dehydrogenase
Source: https://link.springer.com/article/10.1134/S0012496622040056
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