Hyperpolarization Activated Cyclic Nucleotide-Gated Potassium Channel 2 (HCN2) ELISA Kits

Human Hyperpolarization Activated Cyclic Nucleotide-Gated Potassium Channel 2 (HCN2) interaction partners

1. No significant association was found between HCN1/HCN2 alleles, genotypes or haplotypes, and drug resistance in patients, however, it was suggested that HCN2 rs3752158 is involved in the susceptibility to juvenile myoclonic epilepsy.

2. Data suggest that HCN2 variants can confer susceptibility to Genetic generalized epilepsy via a gain-of-function mechanism.

3. beta2-adrenoceptors alone strongly enhanced the activity of HCN2 channels, and co-expression of odorant receptors further diversified the HCN2 channel activity.

4. TRIP8b competes with a portion of the cAMP-binding site or distorts the binding site by making interactions with the binding pocket, thus acting predominantly as a competitive antagonist that inhibits the cyclic-nucleotide dependence of HCN channels.

5. HCN2 has a role in maturation and processing of the amyloid precursor protein

6. promoter methylation status does not appear to be a major determinant of HCN2 expression in normal and adenoid cystic carcinoma ( ACC )tissues. HCN2 hypomethylation is a biomarker of ACC and may play an important role in the carcinogenesis of ACC.

7. 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.

8. Data show that Rab8b-interacting protein TRIP8b does not compete with cyclic AMP for the same binding region of hyperpolarization activated cyclic nucleotide gated potassium channel 2 (HCN2).

9. N-glycosylation is not required for HCN2 channels to function.

10. Thermal hyperalgesia under chronic inflammatory conditions is mediated by HCN2 channels.

11. Novel HCN2 mutation contributes to febrile seizures by shifting the channel's kinetics in a temperature-dependent manner.

12. HCN2 polymorphism may play a role in chronic inflammatory periodontitis but not in peri-implantitis.

13. LBB-injected HCN2/SkM1 potentially provides a more clinically suitable biological pacemaker strategy than other reported constructs. This superiority is attributable to the more negative AP threshold and injection into the LBB

14. HCN2 channels make an important contribution to the maintenance of spontaneous burst activity in embryonic cortical neuron cultures.

15. This is the first evidence in humans for a single-point, homozygous loss-of-function mutation in HCN2 potentially associated with generalized epilepsy with recessive inheritance.

16. Genetic analysis in 48 Sudden unexpected death in epilepsy cases identified six novel and three previously reported nonsynonymous (amino acid changing) variants in HCN1 , HCN2, HCN3 and HCN4.

17. HCN4 activates substantially slower than HCN2 and with a half-maximum activation voltage approximately equal 10 mV less negative, both isoforms activate more positively in myocytes suggesting cell-type specificity

18. activation of the fast channel HCN2 is dependent on the S1 segment

19. HCN1 and HCN2 expression were measured using in situ hybridization and immunocytochemistry in hippocampi; the expression of HCN isoforms is dynamically regulated in human as well as in experimental hippocampal epilepsy

20. Native I(f) channels in atrial myocardium are heteromeric complexes composed of HCN4 and/or HCN2.

Mouse (Murine) Hyperpolarization Activated Cyclic Nucleotide-Gated Potassium Channel 2 (HCN2) interaction partners

1. A mutant channel containing just five mutations (M485I, G497D, S514T, V562A, and S563G) switches cAMP sensitivity of full-length HCN2 to that of HCN1 channels.

2. rescues nicotine-exposed Xenopus embryos, restoring the endogenous bioelectric prepatterns necessary for brain patterning, resulting in normal brain morphology

3. Together, these results reveal a critical role for HCN2 in regulating ventral tegmental area dopamine neuronal activity and depressive-related behaviors.

4. the increased intracellular cAMP drives diabetes-associated pain by facilitating HCN2 activation and consequently promoting repetitive firing in primary nociceptive nerve fibers.

5. The data of this study strongly suggest that cAMP acts by PKA-mediated regulation of HCN2 channel activity and thereby generates nociceptive sensitization.

6. loss via insertion mutation leads to delayed gastrointestinal motility and reduced energy intake

7. Data support a model in which the degree of facilitation of opening in the full-length HCN2 channel by a given ligand depends upon its ability to promote oligomerization of the C-linker/cyclic nucleotide-binding domain in solution.

8. Mouse HCN2-expressing human mesenchymal stem cells are relevant biological models for the generation of biological pacemakers.

9. the allosteric mechanism of different cyclic nucleotides on the cyclic nucleotide-binding domain of HCN2 and on channel gating, was investigated.

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

11. HCN2 channel activity reduces the repolarization reserve of the ventricular action potential and increases ectopic automaticity under pathological conditions such as excessive beta-adrenergic stimulation.

12. This study demonstrated that Increased expression of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in reactive astrocytes following ischemia.

13. fisetin is a partial agonist for HCN2 channels.

14. HCN2 channel expression increases significantly during pregnancy, accelerating the heart rate.

15. cAMP-dependent changes in the structure of the C-helix of a C-terminal fragment of HCN2 channels

16. Dendritic expression of the h-channel subunit HCN1, but not HCN2, was higher in the CA1 region of fmr1(-/y) mice.

17. Leucine zipper motif essential for gating of HCN1 and HCN2.

18. Data indicate that HCN1 and HCN2 form alternate ternary protein complexes with hair-cell stereociliary proteins.

19. Loss of KCNE2 leads to downregulation of HCN channel function associated with increased excitability in neurons in the cortico-thalamo-cortical loop.

20. 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.