Amino acid transport system A (SNAT2) in Chinese hamster ovary (CHO-K1) cells was stimulated when the cells were depleted of amino acids or subjected to hypertonic stress. Each of these stresses also caused increases in the abundance of SNAT2 mRNA in these cells. Similar results were obtained with Madin-Darby canine kidney (MDCK) cells, porcine pulmonary artery endothelial cells and human WI-38 fibroblasts. We conclude that the cellular signal transduction pathways for hypertonic stress and amino acid starvation must converge at or before transcription of the message for SNAT2.
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