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HCN4 encodes a member of the hyperpolarization-activated cyclic nucleotide-gated potassium channels. Additionally we are shipping HCN4 Antibodies (91) and HCN4 Proteins (7) and many more products for this protein.
Showing 4 out of 14 products:
A novel splice site HCN4 gene mutation was identified in a large family with familial bradycardia.
Sick sinus syndrome (SSS) with HCN4 mutations may form a distinct SSS subgroup characterized by early clinical manifestation after adolescence and frequent association with atrial fibrillation and left ventricular noncompaction.
This study has identified 4 synonymous variants in the HCN4 gene and 3 SNPs in the CYP3A4 (show CYP3A4 ELISA Kits) gene. None of the variants appear to have a major effect on the reduction of HR produced by ivabradine.
HCN4 channel remodeling following exercise and subsequent sinus bradycardia in athletes is controlled by miR (show MLXIP ELISA Kits)-423-5p.
Our results indicate that HCN4 channel function is modulated by cav-3 (show CAV3 ELISA Kits). LQTS-associated mutations of cav-3 (show CAV3 ELISA Kits) differentially influence pacemaker current properties indicating a pathophysiological role in clinical manifestations.
Identified in Brugada syndrome patient HCN4 mutation results in reduced channel function in HEK293 cells.
S672R mutation results in a constitutive shift of the dynamic auto-inhibitory equilibrium toward inactive states of HCN4 and broadens the free-energy well of the apo (show C9orf3 ELISA Kits)-form, enhancing the millisecond to microsecond dynamics of the holo-form at sites critical for gating cAMP binding.
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 channels
HCN4-overexpressing mouse embryonic stem cell -derived cardiomyocytes produce rapid ectopic ventricular rhythms as a biological pacemaker.
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.
This study demonstrated that HCN4 regulate the glutamate (show GRIN1 ELISA Kits) release from presynaptic terminals that target excitatory, but not inhibitory spinal substantia gelatinosa interneurons.
Data show that prostaglandin E2 receptor EP3 subtype (EP3 (show PTGER3 ELISA Kits)) was expressed in the interstitial cells of Cajal (ICCs) of the bladder and activated hyperpolarization-activated cyclic nucleotide-gated (HCN) channels.
that hyperpolarization-activated cyclic nucleotide-gated cation channel 4 (HCN4) expression was significantly higher and HCN2 (show HCN2 ELISA Kits) expression was significantly lower in fetal day 13 mice than in adults
beating rate of hiPSC-CMs (show Cd2ap ELISA Kits) co-cultured with aggregates of HCN4-overexpressing mESC-CMs (show Cd2ap ELISA Kits) was significantly higher than that of non-treated hiPSC-CMs (show Cd2ap ELISA Kits) and that of hiPSC-CMs (show Cd2ap ELISA Kits) co-cultured with aggregates of non-overexpressing mESC-CMs (show Cd2ap ELISA Kits)
HCN1, HCN2 (show HCN2 ELISA Kits), and HCN4 subunits may have distinct physiological roles in the developing hippocampus.
Shox2 regulates dorsal mesenchymal protrusion fate and development by controlling BMP signaling through the Smad (show SMAD1 ELISA Kits)-dependent pathway to drive tissue growth and to induce Hcn4 expression
HCN4 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 ELISA Kits) and HCN4 genes.
Data suggest that TRPM7 (show TRPM7 ELISA Kits) influences diastolic membrane depolarization and automaticity in embryonic myocardium and sinoatrial node (SAN) indirectly via regulation of Hcn4 expression.
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