The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

I (K1) and I (f) in ventricular myocytes isolated from control and hypertrophied rat hearts.

Electrophysiological properties of inward rectifier potassium current (I (K1)) and hyperpolarization-activated inward current (I (f)) and the protein expression of the Kir2.1 subfamily and the hyperpolarization- activated cation channel 2 (HCN2) and HCN4 were studied in control and hypertrophied myocytes. Electrophysiological experiments were conducted by whole-cell patch-clamp technique, and protein levels of Kir2.1 subfamily and HCN2 and HCN4 isoforms were analysed by Western blot technique. The density of I (f) as well as the protein expression levels of the HCN2 isoform was found to be significantly higher in hypertrophied myocytes, whereas the protein expression level of HCN4 was not detected in any group. I (K1) density and Kir 2.1 protein expression were similar in control and hypertrophied myocytes, but the time-course of the currents was slower in hypertrophied myocytes. Analysis of I (f) and I (K1) in the same control and hypertrophied myocyte at -80 mV showed that cells in which I (f) was present had values of I (K1) density similar to those cells in which I (f) was not observed. In conclusion, although left ventricular hypertrophy involves an up-regulation of I (f) and its molecular correlate HCN2 in the rat ventricle, its contribution to diastolic depolarization would be limited by the low values of I (f) density at potentials close to the resting potential of the ventricular cells.[1]


  1. I (K1) and I (f) in ventricular myocytes isolated from control and hypertrophied rat hearts. Fernández-Velasco, M., Ruiz-Hurtado, G., Delgado, C. Pflugers Arch. (2006) [Pubmed]
WikiGenes - Universities