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HCN4 encodes a member of the hyperpolarization-activated cyclic nucleotide-gated potassium channels. Additionally we are shipping HCN4 Proteins (7) and HCN4 Kits (5) and many more products for this protein.
Showing 10 out of 54 products:
Human Monoclonal HCN4 Primary Antibody for ICC, IF - ABIN2482541
Zong, Eckert, Yuan, Wahl-Schott, Abicht, Fang, Li, Mistrik, Gerstner, Much, Baumann, Michalakis, Zeng, Chen, Biel: A novel mechanism of modulation of hyperpolarization-activated cyclic nucleotide-gated channels by Src kinase. in The Journal of biological chemistry 2005
Human Polyclonal HCN4 Primary Antibody for IF (p), IHC (p) - ABIN733043
Li, Hong, Zhang, Zhou, Ji, Li, Hu, Li, Sun, Zhang, Xin, Yusufuaji, Xiong, Tang: Association between reversal in the expression of hyperpolarization-activated cyclic nucleotide-gated (HCN) channel and age-related atrial fibrillation. in Medical science monitor : international medical journal of experimental and clinical research 2014
Our results confirm the genetic evidence for the involvement of the HCN4 mutations in the combined bradycardia-non compaction cardiomyopathy phenotype and illustrates that.
Aged patients with sinus rhythm exhibited significantly higher expression levels of HCN2 and HCN4 channel mRNA and protein (P<0.05), but significantly lower expression levels of miR1 and 133, compared with those of adult patients with sinus rhythm.
study establishes the role of f-channels in cardiac automaticity and indicates that arrhythmia related to HCN loss-of-function may be managed by pharmacological or genetic inhibition of GIRK4 (show KCNJ5 Antibodies) channels
The study analyzed HCN4 intracellular region dynamics in the four states of the thermodynamic cycle arising from the coupling between cAMP binding and tetramerization equilibria.
study identified a novel trafficking-defective mutation in the amino-terminus of HCN4 channel in individuals with early-onset atrial fibrillation (AF); findings support that novel loss-of-function mutations in the HCN4 channel may increase susceptibility and have a role in AF pathogenesis
used NMR to probe the changes caused by the binding of cAMP and of cCMP, a partial agonist, to the apo (show C9orf3 Antibodies)-cAMP-binding domain of HCN4
Here, we review the changes in expression and kinetics of HCN4 mutant channels and provide an overview of their effects on If during the time course of a human SAN action potential, both under resting conditions and upon adrenergic stimulation. [review]
The HCN4-G1097W mutant channels displayed a loss-of-function type modulation on cardiac If channels and thus could predispose them to AV nodal dysfunction. These data provide a novel insight into the genetic basis for the AV block.
Mutations in ion channel gene HCN4 may be associated with structural abnormalities of the myocardium.
The symptom complex of sinus node dysfunction and noncompaction cardiomyopathy is associated with heritable HCN4 defects.
Ischemia-reperfusion is harmful to the sinoatrial node and reduces the expression of HCN4.
SAP97 contributes to isoform specific organization of HCN channels within specific domains in the sinoatrial node of the rabbit.
HCN protein expression in the rabbit pacemaker region, was investigated.
beating rate of hiPSC-CMs (show Cd2ap Antibodies) co-cultured with aggregates of HCN4 (show HCN3 Antibodies)-overexpressing mESC-CMs (show Cd2ap Antibodies) was significantly higher than that of non-treated hiPSC-CMs (show Cd2ap Antibodies) and that of hiPSC-CMs (show Cd2ap Antibodies) co-cultured with aggregates of non-overexpressing mESC-CMs (show Cd2ap Antibodies)
HCN1 (show HCN1 Antibodies), HCN2 (show HCN2 Antibodies), and HCN4 (show HCN3 Antibodies) subunits may have distinct physiological roles in the developing hippocampus.
Shox2 (show SHOX2 Antibodies) regulates dorsal mesenchymal protrusion fate and development by controlling BMP signaling through the Smad (show SMAD1 Antibodies)-dependent pathway to drive tissue growth and to induce Hcn4 (show HCN3 Antibodies) expression
HCN4 (show HCN3 Antibodies) dynamically marks the first heart field and conduction system precursors.
testosterone induced cardiomyogenesis, at least in part, by recruiting the AR receptor to the regulatory regions of the MEF2C (show MEF2C Antibodies) and HCN4 (show HCN3 Antibodies) genes.
Data suggest that TRPM7 (show TRPM7 Antibodies) influences diastolic membrane depolarization and automaticity in embryonic myocardium and sinoatrial node (SAN) indirectly via regulation of Hcn4 (show HCN3 Antibodies) expression.
Cardiomyogenic progenitors derived from the first heart field and human pluripotent stem cells express HCN4 (show HCN3 Antibodies).
Spatiotemporal regulation of an Hcn4 (show HCN3 Antibodies) enhancer defines a role for Mef2c (show MEF2C Antibodies) and HDACs in cardiac electrical patterning.
Suggest that the strongly increased HCN channel activity in hypertrophied myocytes prolongs the repolarization of the ventricular action potential and thereby may increase the arrhythmogenic potential.
This gene encodes a member of the hyperpolarization-activated cyclic nucleotide-gated potassium channels. The encoded protein shows slow kinetics of activation and inactivation, and is necessary for the cardiac pacemaking process. This channel may also mediate responses to sour stimuli. Mutations in this gene have been linked to sick sinus syndrome 2, also known as atrial fibrillation with bradyarrhythmia or familial sinus bradycardia. Two pseudogenes have been identified on chromosome 15.
hyperpolarization activated cyclic nucleotide-gated potassium channel 4
, hyperpolarization activated cyclic nucleotide-gated cation channel 4
, potassium/sodium hyperpolarization-activated cyclic nucleotide-gated channel 4
, hyperpolarization-activated, cyclic nucleotide-gated K+ 4
, hyperpolarization activated cation channel
, hyperpolarization-activated cation channel 4
, brain cyclic nucleotide-gated channel 3
, hyperpolarization-activated, cyclic nucleotide-gated K+ 3