Modulation of BKCa channel gating by endogenous signaling molecules.
Large-conductance Ca(2+)- and voltage-activated K(+) (BK(Ca), MaxiK, or Slo1) channels are expressed in almost every tissue in our body and participate in many critical functions such as neuronal excitability, vascular tone regulation, and neurotransmitter release. The functional versatility of BK(Ca) channels owes in part to the availability of a spectacularly wide array of biological modulators of the channel function. In this review, we focus on modulation of BK(Ca) channels by small endogenous molecules, emphasizing their molecular mechanisms. The mechanistic information available from studies on the small naturally occurring modulators is expected to contribute to our understanding of the physiological and pathophysiological roles of BK(Ca) channels.
Hou
Shangwei
S
Department of Physiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Heinemann
Stefan H
SH
Hoshi
Toshinori
T
D000818:Animals; D001685:Biological Factors / Q000378:metabolism / Q000502:physiology*; D002248:Carbon Monoxide / Q000502:physiology; D005227:Fatty Acids / Q000502:physiology; D006418:Heme / Q000502:physiology; D006801:Humans; D051036:Large-Conductance Calcium-Activated Potassium Channels / Q000737:chemistry / Q000378:metabolism* / Q000502:physiology*; D011522:Protons; D015398:Signal Transduction / Q000502:physiology*
D001685:Biological Factors; D005227:Fatty Acids; D051036:Large-Conductance Calcium-Activated Potassium Channels; D011522:Protons; D006418:Heme; D002248:Carbon Monoxide