Dex-ras1 and Serum- and Glucocorticoid-inducible Protein Kinase 1: Regulation of Expression by Dexamethasone in HEK293 Cells |
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Authors: | Ghassem Attarzadeh-Yazdi Michael J Shipston Ferenc A Antoni |
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Institution: | (1) Membrane Biology Group, Centre for Integrative Physiology, University of Edinburgh, Edinburgh, EH8 9XD, UK |
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Abstract: | The molecular and cellular basis of the psychotropic actions of adrenal corticosteroids is poorly understood. Previously,
we reported that modulation of large conductance Ca2+-activated potassium channel (BK-channel) function by glucocorticoids can be recapitulated in human embryonic kidney293 (HEK293)
cells (J Physiol 537:57, 2001). In the present paper, we examined the effect of dexamethasone on the expression of candidate
mediator proteins of glucocorticoid action, dex-ras1 and serum and glucocorticoid inducible protein kinase 1 (SGK), in HEK293
cells. Dex-ras1 mRNA was readily detectable under basal conditions however, no changes of dex-ras1 mRNA expression occurred
upon exposure to 100 nM of dexamethasone for 2 h. In contrast, a 2.5-fold increase of SGK mRNA was found under similar conditions.
Total levels of cellular SGK protein were unaltered upon exposure to dexamethasone, but a marked increase of SGK in a Triton-X100
insoluble fraction was observed. BK-channel α-subunits could not be co-immunoprecipitated with SGK. In summary, SGK, but not
dex-ras1, mRNA is rapidly induced by glucocorticoid stimulation in HEK293 cells. However, there appears to be no direct protein-protein
interaction between SGK and BK-channel α-subunits.
Presented to mark the 70th birthday of Professor George Fink.
Special issue article in honor of George Fink. |
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