Under hypertonic conditions the induction of SLC38A2/SNAT2 leads to the stimulation of transport system A and to the increase in the cell content of amino acids. In hypertonically stressed human fibroblasts transfection with two si- RNAs for SNAT2 suppressed the increase in SNAT2 mRNA and the stimulation of system A transport activity. Under the same condition, the expansion of the intracellular amino acid pool was significantly lowered and cell volume recovery markedly delayed. It is concluded that the up-regulation of SNAT2 is essential for the rapid restoration of cell volume after hypertonic stress.

SNAT2 silencing prevents the osmotic induction of transport system A and hinders cell recovery from hypertonic stress / Bevilacqua, E.; Bussolati, Ovidio; Dall'Asta, Valeria; Gaccioli, F.; Sala, Roberto; Gazzola, Giancarlo; Franchi, Renata. - In: FEBS LETTERS. - ISSN 0014-5793. - 579:(2005), pp. 3376-3380. [10.1016/j.febslet.2005.05.002]

SNAT2 silencing prevents the osmotic induction of transport system A and hinders cell recovery from hypertonic stress

BUSSOLATI, Ovidio;DALL'ASTA, Valeria;SALA, Roberto;GAZZOLA, Giancarlo;FRANCHI, Renata
2005-01-01

Abstract

Under hypertonic conditions the induction of SLC38A2/SNAT2 leads to the stimulation of transport system A and to the increase in the cell content of amino acids. In hypertonically stressed human fibroblasts transfection with two si- RNAs for SNAT2 suppressed the increase in SNAT2 mRNA and the stimulation of system A transport activity. Under the same condition, the expansion of the intracellular amino acid pool was significantly lowered and cell volume recovery markedly delayed. It is concluded that the up-regulation of SNAT2 is essential for the rapid restoration of cell volume after hypertonic stress.
2005
SNAT2 silencing prevents the osmotic induction of transport system A and hinders cell recovery from hypertonic stress / Bevilacqua, E.; Bussolati, Ovidio; Dall'Asta, Valeria; Gaccioli, F.; Sala, Roberto; Gazzola, Giancarlo; Franchi, Renata. - In: FEBS LETTERS. - ISSN 0014-5793. - 579:(2005), pp. 3376-3380. [10.1016/j.febslet.2005.05.002]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11381/1494235
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