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J Biol Chem, Vol. 275, Issue 9, 6090-6100, March 3, 2000
From We describe here several novel properties of the
human The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF126966 (
Molecular and Functional Properties of the Human
1G Subunit That Forms T-type Calcium Channels*
§,,,
, and
IGH-CNRS UPR 1142, 141 rue de la Cardonille,
F-34396 Montpellier cedex 05, France and ¶ CNRS, UMR 5825, Université de Montpellier II,
F-34095 Montpellier cedex 05, France
1G subunit that forms T-type calcium
channels. The partial intron/exon structure of the corresponding gene
CACNA1G was defined and several 1G isoforms
were identified, especially two isoforms that exhibit a distinct III-IV
loop: 1G-a and 1G-b. Northern blot and
dot blot analyses indicated that 1G mRNA is
predominantly expressed in the brain, especially in thalamus,
cerebellum, and substantia nigra. Additional experiments have also
provided evidence that 1G mRNA is expressed at a
higher level during fetal life in nonneuronal tissues (i.e.
kidney, heart, and lung). Functional expression in HEK 293 cells of a
full-length cDNA encoding the shortest 1G isoform
identified to date, 1G-b, resulted in transient, low threshold activated Ca2+ currents with the expected
permeability ratio (ISr > ICa 
IBa) and channel
conductance (~7 pS). These properties, together with slowly
deactivating tail currents, are typical of those of native T-type
Ca2+ channels. This 1G-related current was
inhibited by mibefradil (IC50 = 2 µM) and
weakly blocked by Ni2+ ions (IC50 = 148 µM) and amiloride (IC50 > 1 mM).
We showed that steady state activation and inactivation properties of
this current can generate a "window current" in the range of 
65
to 55 mV. Using neuronal action potential waveforms, we show that
1G channels produce a massive and sustained
Ca2+ influx due to their slow deactivation properties.
These latter properties would account for the specificity of
Ca2+ influx via T-type channels that occurs in the range of
physiological resting membrane potentials, differing considerably from
the behavior of other Ca2+ channels.
*
This work was supported in part by the Program Génome
du CNRS, Association pour la Recherche contre le Cancer Grant ARC9011, and Association Française contre les myopathies.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
1G-a) and AF126965
(1G-b).
To whom correspondence should be addressed. Tel.: 33 499 61 99 36; Fax: 33 499 61 99 01; E-mail: philippe.lory@igh.cnrs.fr.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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