anti-Hyperpolarization Activated Cyclic Nucleotide-Gated Potassium Channel 4 (HCN4) Antibodies

Human Hyperpolarization Activated Cyclic Nucleotide-Gated Potassium Channel 4 (HCN4) interaction partners

1. We here report on multiple families harboring HCN4 mutations, who show significant dilation of the aorta ascendens

2. A novel splice site HCN4 gene mutation was identified in a large family with familial bradycardia.

3. 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.

4. This study has identified 4 synonymous variants in the HCN4 gene and 3 SNPs in the CYP3A4 (show CYP3A4 Antibodies) gene. None of the variants appear to have a major effect on the reduction of HR produced by ivabradine.

5. HCN4 channel remodeling following exercise and subsequent sinus bradycardia in athletes is controlled by miR (show MLXIP Antibodies)-423-5p.

6. Our results indicate that HCN4 channel function is modulated by cav-3 (show CAV3 Antibodies). LQTS-associated mutations of cav-3 (show CAV3 Antibodies) differentially influence pacemaker current properties indicating a pathophysiological role in clinical manifestations.

7. Identified in Brugada syndrome patient HCN4 mutation results in reduced channel function in HEK293 cells.

8. 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 Antibodies)-form, enhancing the millisecond to microsecond dynamics of the holo-form at sites critical for gating cAMP binding.

9. Our results confirm the genetic evidence for the involvement of the HCN4 mutations in the combined bradycardia-non compaction cardiomyopathy phenotype and illustrates that.

10. 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.

Rabbit Hyperpolarization Activated Cyclic Nucleotide-Gated Potassium Channel 4 (HCN4) interaction partners

1. HCN4-overexpressing mouse embryonic stem cell -derived cardiomyocytes produce rapid ectopic ventricular rhythms as a biological pacemaker.

2. Ischemia-reperfusion is harmful to the sinoatrial node and reduces the expression of HCN4.

3. SAP97 contributes to isoform specific organization of HCN channels within specific domains in the sinoatrial node of the rabbit.

4. HCN protein expression in the rabbit pacemaker region, was investigated.

Mouse (Murine) Hyperpolarization Activated Cyclic Nucleotide-Gated Potassium Channel 4 (HCN4) interaction partners

1. This study demonstrated that HCN4 (show HCN3 Antibodies) regulate the glutamate (show GRIN1 Antibodies) release from presynaptic terminals that target excitatory, but not inhibitory spinal substantia gelatinosa interneurons.

2. Data show that prostaglandin E2 receptor EP3 subtype (EP3 (show PTGER3 Antibodies)) was expressed in the interstitial cells of Cajal (ICCs) of the bladder and activated hyperpolarization-activated cyclic nucleotide-gated (HCN) channels.

3. that hyperpolarization-activated cyclic nucleotide-gated cation channel 4 (HCN4) expression was significantly higher and HCN2 (show HCN2 Antibodies) expression was significantly lower in fetal day 13 mice than in adults

4. 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)

5. 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

6. HCN1 (show HCN1 Antibodies), HCN2 (show HCN2 Antibodies), and HCN4 (show HCN3 Antibodies) subunits may have distinct physiological roles in the developing hippocampus.

7. 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

8. HCN4 (show HCN3 Antibodies) dynamically marks the first heart field and conduction system precursors.

9. 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.

10. 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.