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Hyperpolarization activated cyclic nucleotide-gated potassium channel 2

Hyperpolarization-activated cation channels of the HCN gene family, such as HCN2, contribute to spontaneous rhythmic activity in both heart and brain.[supplied by OMIM, Jul 2010] (from NCBI)
Top mentioned proteins: HCN1, HCN4, CAN, HAD, V1a
Papers on HCN2
Structure and Energetics of Allosteric Regulation of HCN2 Ion Channels by Cyclic Nucleotides.
Stoll et al., Seattle, United States. In J Biol Chem, Feb 2016
Hyperpolarization-activated cyclic nucleotide-gated (HCN) ion channels play an important role in regulating electrical activity in the heart and brain.
Fluoxetine ameliorates cognitive impairments induced by chronic cerebral hypoperfusion via down-regulation of HCN2 surface expression in the hippocampal CA1 area in rats.
Guo et al., Wuhan, China. In Pharmacol Biochem Behav, Jan 2016
Furthermore, 2VO caused an up-regulation of hyperpolarization-activated cyclic nucleotide-gated channel 2 (HCN2) surface expressions in the hippocampal CA1 area and fluoxetine also effectively recovered the disorder of HCN2 surface expressions, which may be a possible mechanism that fluoxetine treatment ameliorates cognitive impairments in rats with CCH.
Conformational Flip of Nonactivated HCN2 Channel Subunits Evoked by Cyclic Nucleotides.
Benndorf et al., Jena, Germany. In Biophys J, Jan 2016
Using fcAMP, a fluorescent derivative of cAMP, we analyzed the effect of ligand binding on HCN2 channels not preactivated by voltage.
The hyperpolarization-activated cyclic nucleotide-gated (HCN) channels contain multiple S-palmitoylation sites.
Takano et al., Kurume, Japan. In J Physiol Sci, Dec 2015
Thus, we performed an acyl-biotinyl exchange assay, and found that HCN1, HCN2, and HCN4, but not HCN3, were S-palmitoylated in HEK293 cells.
An N-terminal deletion variant of HCN1 in the epileptic WAG/Rij strain modulates HCN current densities.
Decher et al., Marburg an der Lahn, Germany. In Front Mol Neurosci, 2014
Using co-expression experiments, we found that WAG-HCN1 channels suppress heteromeric HCN2 and HCN4 currents.
Cortical HCN channels: function, trafficking and plasticity.
Shah, London, United Kingdom. In J Physiol, 2014
Four HCN subunits have been cloned, of which HCN1 and HCN2 subunits are predominantly expressed in the cortex.
Differential distribution of voltage-gated channels in myelinated and unmyelinated baroreceptor afferents.
Kunze et al., Indianapolis, United States. In Auton Neurosci, 2013
Interestingly, HCN2 and HCN4 expression levels are comparable in both fiber types.
A biophysical signature of network affiliation and sensory processing in mitral cells.
Margrie et al., London, United Kingdom. In Nature, 2012
This is corroborated by a mosaic, glomerulus-based pattern of expression of the HCN2 (hyperpolarization-activated cyclic nucleotide-gated channel 2) subunit of the Ih channel.
HCN2 ion channels: an emerging role as the pacemakers of pain.
McNaughton et al., Cambridge, United Kingdom. In Trends Pharmacol Sci, 2012
Deletion of the HCN2 isoform from nociceptive neurons abolishes heat-evoked inflammatory pain and all aspects of neuropathic pain, but acute pain sensation is unaffected.
Chronic inflammatory pain is associated with increased excitability and hyperpolarization-activated current (Ih) in C- but not Aδ-nociceptors.
Djouhri et al., Liverpool, United Kingdom. In Pain, 2012
HCN2 channels contribute to inflammation-induced C-nociceptor hyperexcitability in chronic inflammatory pain.
Novel insights into the distribution of cardiac HCN channels: an expression study in the mouse heart.
Ludwig et al., Nürnberg, Germany. In J Mol Cell Cardiol, 2011
HCN2 shows only a confined expression to individual pacemaker cells.
Hyperpolarization-activated cation current contributes to spontaneous network activity in developing neocortical cultures.
Munsch et al., Magdeburg, Germany. In Neurosignals, 2011
HCN2 channels make an important contribution to the maintenance of spontaneous burst activity in embryonic cortical neuron cultures.
Processing of retinal signals in normal and HCN deficient mice.
Gargini et al., Pisa, Italy. In Plos One, 2011
Data show that HCN1 and HCN2 channels are expressed at distinct retinal sites and serve different functions.
Recessive loss-of-function mutation in the pacemaker HCN2 channel causing increased neuronal excitability in a patient with idiopathic generalized epilepsy.
DiFrancesco et al., Monza, Italy. In J Neurosci, 2011
This is the first evidence in humans for a single-point, homozygous loss-of-function mutation in HCN2 potentially associated with generalized epilepsy with recessive inheritance.
HCN2 ion channels play a central role in inflammatory and neuropathic pain.
McNaughton et al., Cambridge, United Kingdom. In Science, 2011
findings show neuropathic pain is initiated by HCN2-driven action potential firing in Na(V)1.8-expressing nociceptors
Mapping the structure and conformational movements of proteins with transition metal ion FRET.
Zagotta et al., Seattle, United States. In Nat Methods, 2009
We used this 'transition metal ion FRET' approach along with X-ray crystallography to determine the structural changes of the gating ring of the mouse hyperpolarization-activated cyclic nucleotide-regulated ion channel HCN2.
Structural basis for modulation and agonist specificity of HCN pacemaker channels.
Gouaux et al., Seattle, United States. In Nature, 2003
X-ray crystallographic structures of C-terminal fragment bound to cAMP or cGMP, identify a tetramerization domain and the mechanism for cyclic nucleotide specificity, and suggest a model for ligand-dependent channel modulation
Molecular mechanism of cAMP modulation of HCN pacemaker channels.
Tibbs et al., New York City, United States. In Nature, 2001
Differences in activation gating and extent of cAMP modulation between the HCN1 and HCN2 isoforms result largely from differences in the efficacy of CNBD inhibition.
Hyperpolarization-Activated Cyclic Nucleotide-Gated (HCN) Ion Channelopathy in Epilepsy
Poolos, Bethesda, United States. In Unknown Journal, 0001
Genetic deletion of the HCN2 channel subtype leads to an absence epilepsy phenotype, while deletion of the HCN1 subtype produces hypersensitivity to provoked seizures and accelerates epileptogenesis.
Perturbations of Dendritic Excitability in Epilepsy
Thompson et al., Bethesda, United States. In Unknown Journal, 0001
epilepsy induced down regulation of Ih (HCN1 and HCN2), and deafferentation induced down regulation of SK-type potassium channels.
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