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

HCN4 encodes a member of the hyperpolarization-activated cyclic nucleotide-gated potassium channels. De plus, nous expédions HCN4 Anticorps (89) et HCN4 Protéines (7) et beaucoup plus de produits pour cette protéine.

list all ELISA KIts Gène GeneID UniProt
HCN4 10021 Q9Y3Q4
HCN4 59266 Q9JKA7
HCN4 330953  
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Catalogue No. Reactivité Sensibilité Gamme Images Quantité Fournisseur Livraison Prix Détails
Humain 0.122 ng/mL 0.31 ng/mL - 20 ng/mL 96 Tests Connectez-vous pour afficher 13 to 16 Days
$736.84
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Souris
  96 Tests Connectez-vous pour afficher 11 to 18 Days
$653.82
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Rat
  96 Tests Connectez-vous pour afficher 15 to 18 Days
$1,029.60
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Plus Kits ELISA pour HCN4 partenaires d'interaction

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

  1. 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.

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

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

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

  5. 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.

  6. 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.

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

  8. 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.

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

  10. 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.

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

  12. 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.

  13. 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

  14. 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.

  15. 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

  16. used NMR to probe the changes caused by the binding of cAMP and of cCMP, a partial agonist, to the apo-cAMP-binding domain of HCN4

  17. 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]

  18. 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.

  19. Mutations in ion channel gene HCN4 may be associated with structural abnormalities of the myocardium.

  20. The symptom complex of sinus node dysfunction and noncompaction cardiomyopathy is associated with heritable HCN4 defects.

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 regulate the glutamate release from presynaptic terminals that target excitatory, but not inhibitory spinal substantia gelatinosa interneurons.

  2. 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.

  3. 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

  4. 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

  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 channels

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

  7. 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

  8. HCN4 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 and HCN4 genes.

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

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

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

  13. 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.

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

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

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

  17. 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.

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

  19. In this review, we focus on genotype-phenotype correlation of HCN4 mutations and discuss the relative contribution of various ion channels to sinus node function.

  20. The expression pattern of HCN isoforms in the olfactory bulb of mice, is described.

HCN4 profil antigène

Antigen Summary

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.

Gene names and symbols associated with HCN4

  • hyperpolarization activated cyclic nucleotide gated potassium channel 4 (HCN4) anticorps
  • hyperpolarization activated cyclic nucleotide gated potassium channel 4 (hcn4) anticorps
  • hyperpolarization activated cyclic nucleotide-gated potassium channel 4 (Hcn4) anticorps
  • hyperpolarization-activated, cyclic nucleotide-gated K+ 4 (Hcn4) anticorps
  • Bcng3 anticorps
  • HAC4 anticorps
  • Hcn3 anticorps
  • SSS2 anticorps

Protein level used designations for HCN4

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 , HAC-4 , hyperpolarization activated cation channel , hyperpolarization-activated cation channel 4 , BCNG-3 , brain cyclic nucleotide-gated channel 3 , hyperpolarization-activated, cyclic nucleotide-gated K+ 3

GENE ID SPECIES
100544822 Meleagris gallopavo
100560546 Anolis carolinensis
10021 Homo sapiens
59266 Rattus norvegicus
785689 Bos taurus
100009452 Oryctolagus cuniculus
330953 Mus musculus
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