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

Christian Derst (First author), E Wischmeyer, R Preisig-Müller, A Spauschus, M Konrad, P Hensen, N Jeck, H W Seyberth, J Daut, A Karschin

    Research output: Contribution to journalOriginal Articlepeer-review

    23 Citations (Web of Science)
    Original languageEnglish
    Pages (from-to)23884-23891
    JournalJOURNAL OF BIOLOGICAL CHEMISTRY
    Volume273
    Issue number37
    Publication statusPublished - 1998

    Keywords

    • INWARD-RECTIFIER
    • K+-CHANNEL
    • BARTTERS-SYNDROME
    • CLONING
    • EXPRESSION
    • PROTEIN
    • BRAIN
    • HYPERCALCIURIA
    • CHROMOSOME-21
    • HETEROGENEITY

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