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Channelopathies (Ionenkanal-Krankheiten) are caused by defects either in an ion conducting or an associated auxiliary subunit of the channel, or by interacting partners. We are focused on structure and function of a voltage-dependent Ca2+-channel containing the Cav2.3 E-type subunit, the formerly called "pharmacoresistant" (R-type) calcium channel. In 1994 the human Cav2.3 was cloned independently in two different groups (Williams M.E. et al., Harpold M.M. & Ellis S.B., 1994 andSchneider T. et al., Stefani E. & Birnbaumer L. 1994). Its gene inactivation in mice has given us access to its physiological function which is related to the cardiac, the endocrine and the neuronal system.

Protein interaction partners of the voltage-gated Ca2+-channel proteins have been detected. They connect ion channel activity with cellular functions helping us to explore molecular mechanisms ofchannelopathies related to arrhythmia, hormone release dysfunction, and neuronal disorders like epilepsy.

 

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