HCN2

HCN2

A gene on chromosome 19p13.3 that encodes a hyperpolarisation-activated cation channels of the HCN gene family, which contributes to spontaneous rhythmic activity in both heart and brain.
References in periodicals archive ?
This then stimulates HCN2 gene ion channels, which triggers nerves to auto-fire (like the pacemakers in the heart).
Ischemia-induced cell depolarization: does the hyperpolarization-activated cation channel HCN2 affect the outcome after stroke in mice?
In human, SAN Hcn4 accounts for 75%, Hcn1 for 21%, Hcn2 for 3%, and Hcn3 for 0.7% of the Hcn in human SAN [53].
Novel approaches for gene-specific interference via manipulating actions of microRNAs: examination on the pacemaker channel genes HCN2 and HCN4.
In summary, our results presented that PTZ induced apoptotic neurodegeneration in HCN2 neuronal cells.
Pan et al., "Down-regulation of miR-1/miR133 contributes to re-expression of pacemaker channel genes HCN2 and HCN4 in hypertrophic heart," Journal of Biological Chemistry, vol.
However, THSG treatment increases the percentage of the S-phase in sorted c-kit(+) rat cardiac stem cells and promotes expressions of PCNA, VEGF, the T-box transcription factor, hyperpolarization-activated cyclic nucleotide-gated 2 (HCN2), HCN4, the a myosin heavy chain, [beta] myosin heavy chain mRNA, stem cell antigen 1, cardiac troponin-I, GATA-4, Nkx2.5, and connexin 43 protein [22].
Benndorf, "Elementary functional properties of single HCN2 channels," Biophysical Journal, vol.
University of Cambridge researchers have isolated a gene called HCN2, which produces a protein that causes chronic pain.
Summary: British scientists have identified a gene responsible for regulating chronic pain, called HCN2, and say their discovery should help drug researchers in their search for more effective, targeted pain-killing medicines.
In neonates, HCN2 and HCN4 subunits are expressed and form channels that are highly sensitive to cAMP and have slower channel dynamics.
Still, mRNA levels of Hcn2, [beta]2-adrenergic receptor, and Bnf, a thyroid hormone-dependent ventricular hypertrophy marker, were raised, along with severe bradycardia, concluding that thyrotoxicosis may have pathological consequences that could continue ahead of the serum T4 level recovery [21].