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A hyperprostaglandin E syndrome mutation in Kir1.1 (renal outer medullary potassium) channels reveals a crucial residue for channel function in Kir1.3 channels.

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Wischmeyer,  E.
Research Group of Molecular Neurobiology of Signal Transduction, MPI for biophysical chemistry, Max Planck Society;

Karschin,  A.
Max Planck Society;

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Citation

Derst, C., Wischmeyer, E., Preisig-Mueller, R., Spauschus, A., Konrad, M., Hensen, P., et al. (1998). A hyperprostaglandin E syndrome mutation in Kir1.1 (renal outer medullary potassium) channels reveals a crucial residue for channel function in Kir1.3 channels. Journal of Biological Chemistry, 273, 23884-23891.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0012-FDA0-7
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