Hyperpolarization Activated Cyclic Nucleotide-Gated Potassium Channel 4 (HCN4) ELISA Kits

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

1. One missense heterozygous variant c.1578C>T (Ala195Val) and four synonymous heterozygous variants c.1552C>T, c.2833C>T, c.3823C>T, and c.4189C>A were discovered in the Sudden unexplained nocturnal death syndrome cases

2. Results found that HCN4 expression level is modulated by GSK3B in neurons.

3. The article described how the structure of the apo cAMP binding domain of the HCN4 isoform has contributed to a model for the cAMP-dependent modulation of the HCN ion-channel. (Review)

4. Human cardiomyocyte progenitor cells expressing HCN4-GFP functionally couple to neonatal rat ventricular myocytes and induce physiologically controlled pacemaker activity and may therefore provide an attractive delivery platform for sustained pacemaker function.

5. The authors report here the first evidence for a heterozygous gain-of-function mutation in the pacemaker HCN4 channel associated with symptoms of familial Inappropriate Sinus Tachycardia.

6. Three HCN4 mutations identified in sick sinus syndrome patients caused loss of function in vitro. Loss of function may have resulted from significantly reduced functional HCN4 channel availability and cell surface expression due to defective trafficking.

7. These findings indicate that HCN4(G811E) may not be a monogenic factor to cause the cardiac disorders.

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

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

10. 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.

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

12. HCN4 channel remodeling following exercise and subsequent sinus bradycardia in athletes is controlled by miR-423-5p.

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

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

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

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

17. 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.

18. 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

19. 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.

20. 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

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. knockdown of HCN4 gave rise to sinus arrhythmia, and enhanced the parasympathetic response.

2. HCN4 is expressed in various regions of the hippocampus. HCN4 knockdown produced no effect on contextual fear conditioning or spatial memory. Anxiogenic effect was evident in mice treated with short hairpin RNA against HCN4.

3. This study demonstrated that HCN4 regulate the glutamate release from presynaptic terminals that target excitatory, but not inhibitory spinal substantia gelatinosa interneurons.

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

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

6. beating rate of hiPSC-CMs co-cultured with aggregates of HCN4-overexpressing mESC-CMs was significantly higher than that of non-treated hiPSC-CMs and that of hiPSC-CMs co-cultured with aggregates of non-overexpressing mESC-CMs

7. 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

8. HCN1, HCN2, and HCN4 subunits may have distinct physiological roles in the developing hippocampus.

9. Shox2 regulates dorsal mesenchymal protrusion fate and development by controlling BMP signaling through the Smad-dependent pathway to drive tissue growth and to induce Hcn4 expression

10. HCN4 dynamically marks the first heart field and conduction system precursors.

11. testosterone induced cardiomyogenesis, at least in part, by recruiting the AR receptor to the regulatory regions of the MEF2C and HCN4 genes.

12. Data suggest that TRPM7 influences diastolic membrane depolarization and automaticity in embryonic myocardium and sinoatrial node (SAN) indirectly via regulation of Hcn4 expression.

13. Cardiomyogenic progenitors derived from the first heart field and human pluripotent stem cells express HCN4.

14. Spatiotemporal regulation of an Hcn4 enhancer defines a role for Mef2c and HDACs in cardiac electrical patterning.

15. 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.

16. The conserved CBD present in all HCN isoforms mediates their functional interaction with caveolins.

17. HCN4 was confirmed as the predominant isoform of the primary pacemaker.

18. HCN4 channels are expressed in different patterns in brain and heart; the N terminus is important for HCN4 channel activation

19. Data show that ablation of HCN4 consistently leads to progressive development of severe bradycardia and AV block, eventually leading to heart arrest and death in about 5 d.

20. HCN4 channels can be regulated by PKA, and this mechanism could contribute to sympathetic regulation of heart rate.