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Inaktivierung des murinen Gens des Hyperpolarisations-aktivierten Zyklonukleotid-gesteuerten Kationenkanals Typ Drei (HCN3)
Inaktivierung des murinen Gens des Hyperpolarisations-aktivierten Zyklonukleotid-gesteuerten Kationenkanals Typ Drei (HCN3)
The hyperpolarization-activated, cyclic-nucleotide-gated cation channel (HCN) familiy comprises four members. The channels play a role in the formation of rhythmic activity of heart and brain. In contrast to the other three members of the HCN channel family, there are only a few studies of tissue distribution and electrophysiological properties of HCN3 so far. Expression has been reported at low levels, but throughout the brain, in some other tissues such as retina, olfactory epithelium and recently in the heart. In order to study the physiological relevance of HCN3 expression, we generated HCN3-deficient mouse lines by gene targeting and homologous recombination: a complete Knockout, a complete Knockout expressing the reporter gene lacZ instead of HCN3 and a conditional Knockout using the Cre-loxP system to study spatial and temporal functions of this pacemaker channel. The functional characterization included behavioural studies and heart physiology.
HCN3, knockout, ion channel, transgenic animal
Mader, Robert
2004
Deutsch
Universitätsbibliothek der Ludwig-Maximilians-Universität München
Mader, Robert (2004): Inaktivierung des murinen Gens des Hyperpolarisations-aktivierten Zyklonukleotid-gesteuerten Kationenkanals Typ Drei (HCN3). Dissertation, LMU München: Fakultät für Chemie und Pharmazie
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Abstract

The hyperpolarization-activated, cyclic-nucleotide-gated cation channel (HCN) familiy comprises four members. The channels play a role in the formation of rhythmic activity of heart and brain. In contrast to the other three members of the HCN channel family, there are only a few studies of tissue distribution and electrophysiological properties of HCN3 so far. Expression has been reported at low levels, but throughout the brain, in some other tissues such as retina, olfactory epithelium and recently in the heart. In order to study the physiological relevance of HCN3 expression, we generated HCN3-deficient mouse lines by gene targeting and homologous recombination: a complete Knockout, a complete Knockout expressing the reporter gene lacZ instead of HCN3 and a conditional Knockout using the Cre-loxP system to study spatial and temporal functions of this pacemaker channel. The functional characterization included behavioural studies and heart physiology.