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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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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0012-FDA0-7 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002A-C5DC-E
Genre: Journal Article

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 Creators:
Derst, C., Author
Wischmeyer, E.1, Author              
Preisig-Mueller, R., Author
Spauschus, A., Author
Konrad, M., Author
Hensen, P., Author
Jeck, N., Author
Seyberth, H. W., Author
Daut, J., Author
Karschin, A.2, Author
Affiliations:
1Research Group of Molecular Neurobiology of Signal Transduction, MPI for biophysical chemistry, Max Planck Society, ou_578561              
2Max Planck Society, ou_persistent13              

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Language(s): eng - English
 Dates: 1998
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Method: -
 Identifiers: eDoc: 233195
Other: 811
 Degree: -

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Title: Journal of Biological Chemistry
Source Genre: Journal
 Creator(s):
Affiliations:
Publ. Info: -
Pages: - Volume / Issue: 273 Sequence Number: - Start / End Page: 23884 - 23891 Identifier: -