The fast and slow ups and downs of HCN channel regulation

Alan S. Lewis; Chad M. Estep; Dane M. Chetkovich

doi:10.4161/chan.4.3.11630

The fast and slow ups and downs of HCN channel regulation

Alan S. Lewis, Chad M. Estep, Dane M. Chetkovich

Neurology

Research output: Contribution to journal › Review article › peer-review

35 Scopus citations

Abstract

Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels (h channels) form the molecular basis for the hyperpolarization-activated current, I_h, and modulation of h channels contributes to changes in cellular properties critical for normal functions in the mammalian brain and heart. Numerous mechanisms underlie h channel modulation during both physiological and pathological conditions, leading to distinct changes in gating, kinetics, surface expression, channel conductance or subunit composition of h channels. Here we provide a focused review examining mechanisms of h channel regulation, with an emphasis on recent findings regarding interacting proteins such as TRIP8b. This review is intended to serve as a comprehensive resource for physiologists to provide potential molecular mechanisms underlying functionally important changes in I_h in different biological models, as well as for molecular biologists to delineate the predicted h channel changes associated with complex regulatory mechanisms in both normal function and in disease states.

Original language	English (US)
Journal	Channels
Volume	4
Issue number	3
DOIs	https://doi.org/10.4161/chan.4.3.11630
State	Published - Jan 1 2010

Keywords

Channel trafficking
Epilepsy
HCN channels
I
I
Long QT syndrome
TRIP8b
Voltage-gated ion channel

ASJC Scopus subject areas

Biophysics
Biochemistry

Access to Document

10.4161/chan.4.3.11630

Cite this

@article{6f22716ed756484d9eced321aec98636,

title = "The fast and slow ups and downs of HCN channel regulation",

abstract = "Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels (h channels) form the molecular basis for the hyperpolarization-activated current, Ih, and modulation of h channels contributes to changes in cellular properties critical for normal functions in the mammalian brain and heart. Numerous mechanisms underlie h channel modulation during both physiological and pathological conditions, leading to distinct changes in gating, kinetics, surface expression, channel conductance or subunit composition of h channels. Here we provide a focused review examining mechanisms of h channel regulation, with an emphasis on recent findings regarding interacting proteins such as TRIP8b. This review is intended to serve as a comprehensive resource for physiologists to provide potential molecular mechanisms underlying functionally important changes in Ih in different biological models, as well as for molecular biologists to delineate the predicted h channel changes associated with complex regulatory mechanisms in both normal function and in disease states.",

keywords = "Channel trafficking, Epilepsy, HCN channels, I, I, Long QT syndrome, TRIP8b, Voltage-gated ion channel",

author = "Lewis, {Alan S.} and Estep, {Chad M.} and Chetkovich, {Dane M.}",

note = "Funding Information: This work was supported by National Institutes of Health grants 1F30NS064757 (Alan S. Lewis) and 1K02NS05595 and 1R01NS059934 (Dane M. Chetkovich).",

year = "2010",

month = jan,

day = "1",

doi = "10.4161/chan.4.3.11630",

language = "English (US)",

volume = "4",

journal = "Channels",

issn = "1933-6950",

publisher = "Landes Bioscience",

number = "3",

}

TY - JOUR

T1 - The fast and slow ups and downs of HCN channel regulation

AU - Lewis, Alan S.

AU - Estep, Chad M.

AU - Chetkovich, Dane M.

N1 - Funding Information: This work was supported by National Institutes of Health grants 1F30NS064757 (Alan S. Lewis) and 1K02NS05595 and 1R01NS059934 (Dane M. Chetkovich).

PY - 2010/1/1

Y1 - 2010/1/1

N2 - Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels (h channels) form the molecular basis for the hyperpolarization-activated current, Ih, and modulation of h channels contributes to changes in cellular properties critical for normal functions in the mammalian brain and heart. Numerous mechanisms underlie h channel modulation during both physiological and pathological conditions, leading to distinct changes in gating, kinetics, surface expression, channel conductance or subunit composition of h channels. Here we provide a focused review examining mechanisms of h channel regulation, with an emphasis on recent findings regarding interacting proteins such as TRIP8b. This review is intended to serve as a comprehensive resource for physiologists to provide potential molecular mechanisms underlying functionally important changes in Ih in different biological models, as well as for molecular biologists to delineate the predicted h channel changes associated with complex regulatory mechanisms in both normal function and in disease states.

AB - Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels (h channels) form the molecular basis for the hyperpolarization-activated current, Ih, and modulation of h channels contributes to changes in cellular properties critical for normal functions in the mammalian brain and heart. Numerous mechanisms underlie h channel modulation during both physiological and pathological conditions, leading to distinct changes in gating, kinetics, surface expression, channel conductance or subunit composition of h channels. Here we provide a focused review examining mechanisms of h channel regulation, with an emphasis on recent findings regarding interacting proteins such as TRIP8b. This review is intended to serve as a comprehensive resource for physiologists to provide potential molecular mechanisms underlying functionally important changes in Ih in different biological models, as well as for molecular biologists to delineate the predicted h channel changes associated with complex regulatory mechanisms in both normal function and in disease states.

KW - Channel trafficking

KW - Epilepsy

KW - HCN channels

KW - I

KW - Long QT syndrome

KW - TRIP8b

KW - Voltage-gated ion channel

UR - http://www.scopus.com/inward/record.url?scp=77953894669&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77953894669&partnerID=8YFLogxK

U2 - 10.4161/chan.4.3.11630

DO - 10.4161/chan.4.3.11630

M3 - Review article

C2 - 20305382

AN - SCOPUS:77953894669

SN - 1933-6950

VL - 4

JO - Channels

JF - Channels

IS - 3

ER -

The fast and slow ups and downs of HCN channel regulation

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this