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Subunits Expressed in Human Embryonic Kidney 293 Cells
Department of Pharmacological and Physiological Sciences, The
University of Chicago, Chicago, Illinois 60637 (L.R.S., R.J.M.),
Department of Biological Chemistry, The University of Michigan, Ann
Arbor, Michigan 48109 (R.T.), and
Eli Lilly Research Laboratories,
Windlesham, UK (S.E.G.)
We examined the ability of different G protein subunits to inhibit the
activity of human 
1B and 1E Ca2+ channels stably
expressed in human embryonic kidney (HEK) 293 cells together with 
1B
and 2B
Ca2+ channel subunits. Under normal
conditions, Ca2+ currents in 1B-expressing cells showed
little facilitation after a depolarizing prepulse. However, when we
overexpressed the 2
2 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 subunits s, i1, and o or with the G protein 2 and 2
subunits alone. Studies carried out in cells expressing 1E currents
showed that overexpression of 22 subunits produced prepulse
facilitation, although this was of lesser magnitude than that observed
with Ca2+ currents in 1B-expressing cells. The subunits
2 and 2 alone produced no effects, nor did constitutively active
s, i1, and o subunits. Phorbol esters enhanced 1E
Ca2+ currents but had no effect on 1B currents,
suggesting that protein kinase C activation was not responsible for the
observed effects. When 1E Ca2+ currents were expressed
without their subunits, they exhibited prepulse facilitation. These
results demonstrate that 1E Ca2+ currents are less
susceptible to direct modulation by G proteins than 1B currents and
illustrate the antagonistic interactions between Ca2+
channel subunits and G proteins.
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