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

Derst, C.; Wischmeyer, E.; Preisig-Mueller, R.; Spauschus, A.; Konrad, M.; Hensen, P.; Jeck, N.; Seyberth, H. W.; Daut, J.; Karschin, A.

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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.

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.

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Datensatz-Permalink: https://hdl.handle.net/11858/00-001M-0000-0012-FDA0-7 Versions-Permalink: https://hdl.handle.net/11858/00-001M-0000-002A-C5DC-E

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Urheber:
Derst, C., Autor
Wischmeyer, E.¹, Autor
Preisig-Mueller, R., Autor
Spauschus, A., Autor
Konrad, M., Autor
Hensen, P., Autor
Jeck, N., Autor
Seyberth, H. W., Autor
Daut, J., Autor
Karschin, A.², Autor

Affiliations:
1Research Group of Molecular Neurobiology of Signal Transduction, MPI for biophysical chemistry, Max Planck Society, ou_578561
2Max Planck Society, ou_persistent13