Inhibition of nuclear import of calcineurin prevents myocardial hypertrophy

Matthias Hallhuber, Natalie Burkard, Rongxue Wu, Mamta H. Buch, Stefan Engelhardt, Lutz Hein, Ludwig Neyses, Kai Schuh, Oliver Ritter

    Research output: Contribution to journalArticlepeer-review


    The time that transcription factors remain nuclear is a major determinant for transcriptional activity. It has recently been demonstrated that the phosphatase calcineurin is translocated to the nucleus with the transcription factor nuclear factor of activated T cells (NF-AT). This study identifies a nuclear localization sequence (NLS) and a nuclear export signal (NES) in the sequence of calcineurin. Furthermore we identified the nuclear cargo protein importinβ1 to be responsible for nuclear translocation of calcineurin. Inhibition of the calcineurin/importin interaction by a competitive peptide (KQECKIKYSERV), which mimicked the calcineurin NLS, prevented nuclear entry of calcineurin. A noninhibitory control peptide did not interfere with the calcineurin/importin binding. Using this approach, we were able to prevent the development of myocardial hypertrophy. In angiotensin II-stimulated cardiomyocytes, [H]-leucine incorporation (159%±9 versus 111%±11; P
    Original languageEnglish
    Pages (from-to)626-635
    Number of pages9
    JournalCirculation research
    Issue number6
    Publication statusPublished - Sep 2006


    • Angiotensin II
    • Calcineurin
    • Gene regulation
    • Hypertrophy
    • NF-AT
    • Nuclear-localizing signals


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