Gating mechanism of a cloned potassium channel expressed in frog oocytes and mammalian cells.
We have cloned a cDNA coding for a delayed rectifier K+ channel from rat brain (RCK1) and rat muscle (RMK1) and expressed it in Xenopus oocytes and in a myoblast cell line (Sol-8). Stably transfected Sol-8 cells exhibited large outward K+ currents, which were indistinguishable from the K+ currents induced in Xenopus oocytes by injection of mRNA transcribed in vitro. RCK1 encodes a K+ channel with a unitary conductance of approximately 14 pS. The steep voltage dependence of channel opening resides in transitions between closed states, whereas the direct transitions into and out of the open state are very rapid and not markedly voltage-dependent. Channel inactivation is very slow, voltage-independent, and occurs from the open state only. We present a simple model that incorporates our findings and is consistent with the presumed structural symmetry of a functional K+ channel.
Koren
G
G
Department of Cellular and Molecular Physiology, Harvard Medical School, Boston, Massachusetts 02115.
Liman
E R
ER
Logothetis
D E
DE
Nadal-Ginard
B
B
Hess
P
P
D000818:Animals; D001921:Brain / Q000648:ultrastructure; D002999:Clone Cells; D003001:Cloning, Molecular; D015870:Gene Expression; D015640:Ion Channel Gating / Q000502:physiology*; D009132:Muscles / Q000648:ultrastructure; D009865:Oocytes / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology*; D051381:Rats; D014981:Xenopus
D015221:Potassium Channels