| First Author | Fan J | Year | 2017 |
| Journal | Channels (Austin) | Volume | 11 |
| Issue | 5 | Pages | 434-443 |
| PubMed ID | 28467171 | Mgi Jnum | J:380270 |
| Mgi Id | MGI:6873610 | Doi | 10.1080/19336950.2017.1326233 |
| Citation | Fan J, et al. (2017) Down-regulation of T-type Cav3.2 channels by hyperpolarization-activated cyclic nucleotide-gated channel 1 (HCN1): Evidence of a signaling complex. Channels (Austin) 11(5):434-443 |
| abstractText | Formation of complexes between ion channels is important for signal processing in the brain. Here we investigate the biochemical and biophysical interactions between HCN1 channels and Cav3.2 T-type channels. We found that HCN1 co-immunoprecipitated with Cav3.2 from lysates of either mouse brain or tsA-201 cells, with the HCN1 N-terminus associating with the Cav3.2 N-terminus. Cav3.2 channel activity appeared to be functionally regulated by HCN1. The expression of HCN1 induced a decrease in Cav3.2 Ba(2+) influx (IBa(2+)) along with altered channel kinetics and a depolarizing shift in activation gating. However, a reciprocal regulation of HCN1 by Cav3.2 was not observed. This study highlights a regulatory role of HCN1 on Cav3.2 voltage-dependent properties, which are expected to affect physiologic functions such as synaptic transmission and cellular excitability. |
