This project is part of the DFG-funded Research Training Group (RTG) “Chemical Biology of Ion Channels (Chembion)“. Ion channels are important cell surface receptors embedded in the plasma membrane and have been known for decades as important and clinically validated drug targets.1 They mediate fast electrical and chemical signalling and, thereby, govern a plethora of physiological functions. Admittedly, the targeted chemical modulation of ion channels is difficult, and compared to G-protein coupled receptors (GPCRs), nuclear receptors, and enzymes, the pharmacological exploitation of ion channels is lagging behind. Due to the membrane embedded nature of ion channels, X-ray structures are not easily accessible. Cryo-EM structures are also of limited use for the design of modulators due to their low resolution. The goal of this project is to provide a detailed understanding of the binding mode of available KCa3.1 channel modulators based on MD simulations, structural modelling, and experimental validation. The results will be used for structure-based design and virtual screening approaches for the development and identification of modulators.
The KCa3.1 channel that belongs to the family of small conductance calcium-activated potassium channels.2 The channel gating mechanism is regulated by calcium binding to calmodulin (CaM), which in turn is bound to a specific CaM binding domain of each of the four subunits. Upon calcium binding, calmodulin interacts with a specific linker region which undergoes a conformational change to open the channel pore. Recently published Cryo-EM structures of the KCa3.1 channel2 not only provide insights of different channel states (closed, Ca2+-bound state I and Ca2+-bound state II), but can also be used for a detailed analysis of the channel and its modulators. In a first computational analysis, we were able to model a senicapoc-based fluorescent probe binding to KCa3.1 channel based on docking.3 In a subsequent study, we could also explain the different behaviour of the KCa3.1 channel staining via the senicapoc-based dye and an antibody-based indirect immunofluorescence labeling.4 A co-staining of both was experimentally not possible and can be explained by the different binding behaviour of both dyes. The senicapoc-based dye binds to the open state and the antibody interacts presumably with the closed state. This explained the impossibility of co-staining.
Currently, a long-term molecular dynamics simulation is running to validate the senicapoc and the dye models and to get more insights into the binding of this fluorescent probe. This should be used to further guide the structure-based design and the development of more active inhibitors and chemical probes for the KCa3.1 channel.
References
- Kurachi, Y., North, A. Ion channels: their structure, function and control – an overview. J. Physiol. 2004, 554, 245–247
- Lee, C.H., MacKinnon, R. Activation mechanism of a human SK-calmodulin channel complex elucidated by cryo-EM structures. Science. 2018, 360, 508-513.
- Brömmel, K., Maskri, S., Maisuls, I., Konken, C.P., Rieke, M., Pethő, Z., Strassert, C.A., Koch, O., Schwab, A., Wünsch, B. Synthesis of small-molecule fluorescent probes for the In vitro imaging of calcium-activated potassium channel KCa 3.1. Angew. Chem. Int. Ed. Engl. 2020, 59, 8277-8284. https://doi.org/10.1002/anie.202001201
- Brömmel, K., Maskri, S., Bulk, E. Pethő, Z., Rieke, M., Budde, T. Koch, O., Schwab, A., Wünsch, B. Co-staining of KCa3.1 channels in NSCLC cells with a small-molecule fluorescent probe and antibody-based indirect immunofluorescence. ChemMedChem 2020, early view. https://doi.org/10.1002/cmdc.202000652