Lee Shekter - Regulation of human neuronal calcium channels by G protein betagamma subunits expressed in human embryonic kidney 293 cells.

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  Publication Details (including relevant citation   information): Shekter,L.R., Taussig,R., Gillard,S.E.,   Miller,R.J., Mol Pharmacol, 1997,   52 (2), pp 282-291

  Abstract: We examined the ability of different G   protein subunits to inhibit the activity of human alpha1B and   alpha1E Ca2+ channels stably expressed in human embryonic kidney   (HEK) 293 cells together with beta1B and alpha2Bdelta Ca2+   channel subunits. Under normal conditions, Ca2+ currents in   alpha1B-expressing cells showed little facilitation after a   depolarizing prepulse. However, when we overexpressed the   beta2gamma2 subunits of heterotrimeric G proteins, the time   course of activation of the Ca2+ currents was considerably slowed   and a depolarizing prepulse produced a large facilitation of the   current as well as an acceleration in its time course of   activation. Similar effects were not observed when cells were   transfected with constitutively active mutants of the G protein   alpha subunits alpha s, alpha i1, and alpha o or with the G   protein beta2 and gamma2 subunits alone. Studies carried out in   cells expressing alpha1E currents showed that overexpression of   beta2gamma2 subunits produced pre-pulse facilitation, although   this was of lesser magnitude than that observed with Ca2+   currents in alpha1B-expressing cells. The subunits beta2 and   gamma2 alone produced no effects, nor did constitutively active   alpha s, alpha i1, and alpha o subunits. Phorbol esters enhanced   alpha1E Ca2+ currents but had no effect on alpha1B currents,   suggesting that protein kinase C activation was not responsible   for the observed effects. When alpha1E Ca2+ currents were   expressed without their beta subunits, they exhibited prepulse   facilitation. These results demonstrate that alpha1E Ca2+   currents are less susceptible to direct modulation by G proteins   than alpha1B currents and illustrate the antagonistic   interactions between Ca2+ channel beta subunits and G proteins.

  Address (URL): http://www.hubmed.org/display.cgi?uids=9271351