Publication: Loss of function mutation of the Slc38a3 glutamine transporter reveals its critical role for amino acid metabolism in the liver, brain, and kidney
Loss of function mutation of the Slc38a3 glutamine transporter reveals its critical role for amino acid metabolism in the liver, brain, and kidney
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Chan, K., Busque, S. M., Sailer, M., Stoeger, C., Bröer, S., Daniel, H., Rubio-Aliaga, I., & Wagner, C. A. (2016). Loss of function mutation of the Slc38a3 glutamine transporter reveals its critical role for amino acid metabolism in the liver, brain, and kidney. Pflügers Archiv : European Journal of Physiology, 468(2), 213–227. https://doi.org/10.1007/s00424-015-1742-0
Abstract
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Glutamine, the most abundant amino acid in mammals, is critical for cell and organ functions. Its metabolism depends on the ability of cells to take up or release glutamine by transporters located in the plasma membrane. Several solute carrier (SLC) families transport glutamine, but the SLC38 family has been thought to be mostly responsible for glutamine transport. We demonstrate that despite the large number of glutamine transporters, the loss of Snat3/Slc38a3 glutamine transporter has a major impact on the function of organs express
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Creators (Authors)
- Chan, Kessara
- Busque, Stephanie M
- Sailer, Manuela
- Stoeger, Claudia
- Bröer, Stefan
- Daniel, Hannelore
- Rubio-Aliaga, Isabel
- Wagner, Carsten A
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Citations
Chan, K., Busque, S. M., Sailer, M., Stoeger, C., Bröer, S., Daniel, H., Rubio-Aliaga, I., & Wagner, C. A. (2016). Loss of function mutation of the Slc38a3 glutamine transporter reveals its critical role for amino acid metabolism in the liver, brain, and kidney. Pflügers Archiv : European Journal of Physiology, 468(2), 213–227. https://doi.org/10.1007/s00424-015-1742-0
