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The membrane protein encoded by HCN1 is a hyperpolarization-activated cation channel that contributes to the native pacemaker currents in heart and neurons. Additionally we are shipping HCN1 Antibodies (96) and many more products for this protein.
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A new mode of regulating HCN1 trafficking: through the use of a di-arginine ER retention signal that monitors processing of the channel in the early secretory pathway.
de novo HCN1 point mutations cause a recognizable early-onset epileptic encephalopathy in humans
acute abrogation of HCN1-FLNa (show FLNA Proteins) interaction in neurons, with the use of decoy peptides that mimic the FLNa (show FLNA Proteins)-binding domain of HCN1, abolishes the punctate distribution of HCN1 channels in neuronal cell bodies
Studies suggest that HCN1 channels may be therapeutic targets for treatment of depressive disorders.
Wild-type presynaptic HCN1 channel function is persistently decreased following seizures.
HCN1 channels make an important contribution to the maintenance of spontaneous burst activity in embryonic cortical neuron cultures.
Hyperpolarization-activated currents are smaller and slower, input resistances are higher, and membrane time constants are longer in HCN1-deficient than in HCN1-expressing neurons of the ventral cochlear nucleus.
Genetic analysis in 48 Sudden unexpected death in epilepsy cases identified six novel and three previously reported nonsynonymous (amino acid changing) variants in HCN1 , HCN2 (show HCN2 Proteins), HCN3 (show HCN3 Proteins) and HCN4 (show HCN4 Proteins).
increasing cAMP levels in cells antagonized the up-regulation of HCN1 channels mediated by a TRIP8b construct binding the CNBD exclusively.
Human HCN1 hyperpolarization activated current (Ih) amplitude is rapidly enhanced after establishment of the whole-cell configuration in HEK293 cells.
in the absence of HCN1-mediated feedback, the amplitude of rod signals remains at high levels for a prolonged period of time, leading to saturation of the retinal pathways.
These results demonstrate that the CB1R (show CNR1 Proteins)-Ih pathway in the hippocampus is obligatory for the action of cannabinoids on long-term potentiation and spatial memory formation.
Resilience to tinnitus is developed in mice that show a re-emergence of KCNQ2/3 channel activity and a reduction in HCN channel activity.
HCN1, HCN2 (show HCN2 Proteins), and HCN4 (show HCN3 Proteins) subunits may have distinct physiological roles in the developing hippocampus.
Forebrain HCN1 channels contribute to hypnotic and amnestic effects of volatile anesthetics, but do not contribute to immobilizing actions.
This study demonstrated that Increased expression of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in reactive astrocytes following ischemia.
Results suggest that spike-and-wave discharges in an established model of absence epilepsy reduce hippocampal HCN1 expression and function, and that the reduction associates with a spatial learning deficit
Grid fields in HCN1 KO mice display more experience-dependent asymmetry consistent with reports of enhanced long-term potentiation in the absence of HCN1. The loss of HCN1 improves temporal coding via the rate-phase transformation.
We conclude that TRIP8b in the retina is needed to achieve maximal expression of HCN1.
HCN1 channels in cerebellar Purkinje cells reduce the duration of inhibitory synaptic responses.
The membrane protein encoded by this gene is a hyperpolarization-activated cation channel that contributes to the native pacemaker currents in heart and neurons. The encoded protein can homodimerize or heterodimerize with other pore-forming subunits to form a potassium channel. This channel may act as a receptor for sour tastes.
hyperpolarization activated cyclic nucleotide-gated potassium channel 1
, brain cyclic nucleotide gated channel 1
, brain cyclic nucleotide-gated channel 1
, potassium/sodium hyperpolarization-activated cyclic nucleotide-gated channel 1
, hyperpolarization-activated cyclic nucleotide-gated channel 1
, hyperpolarization-activated cation channel 2