Modulation of hERG and hEAG K+ channels by small molecules

In the mammalian heart ERG channels (Kv11.1) conduct the rapid delayed rectifier K+ current, IKr. Pathological reduction of IKr is a common side effect of many medications, which can lead to life threatening arrhythmias. In recent years also compounds that activate rather than block hERG have been identified. The potential of these activators for the treatment or prevention of arrhythmias associated with congenital long QT syndrome and specific cancers is widely unexplored.
The aim of this project is to provide detailed insights into the mechanisms underlying hERG small molecule interactions, including investigation of the dynamics of drug-receptor interactions. This is achieved by applying a combination of experimental methods (patch-clamp, site-directed mutagenesis) and computational methods (molecular dynamics simulations, homology modelling and docking methods).

Current Funding:

  • FWF doctoral program "Molecular Drug Targets" grant W1232
  • Grant H-304013/2014 from the Wiener Hochschuljubilaumsstiftung, City of Vienna

Group members:

  • Dr. Anna Weinzinger (Group leader, MolTag faculty member)
  • Mona Abdelghani (visiting student)

 

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