Journal
SCIENCE SIGNALING
Volume 1, Issue 25, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scisignal.125pe31
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Funding
- Howard Hughes Medical Institute Funding Source: Medline
- NHLBI NIH HHS [P01 HL069779, P01 HL069779-06A10003, R01 HL089312-03, R01 HL060562, R01 HL081104, R01 HL081104-04, R01 HL089312, P50 HL077101, R01 HL060562-11, R01 HL033921, R01 HL062927, R37 HL033921, R01 HL062927-10A1, P50 HL077101-050004] Funding Source: Medline
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In noncontractile cells, a sustained increase in total cytoplasmic Ca2+ concentration is typically needed to activate the intracellular protein phosphatase calcineurin, leading to dephosphorylation of the transcription factor nuclear factor of activated T cells (NFAT), its nuclear translocation, and induction of gene expression. It remains a mystery exactly how Ca2+-dependent signaling pathways, such as that mediated by calcineurin-NFAT, are regulated in contracting cardiac myocytes given the highly specialized manner in which Ca2+ concentration rhythmically cycles in excitation-contraction coupling. Here, we critically review evidence that supports the hypothesis that calcineurin-NFAT signaling is regulated by contractile Ca2+ transients in cardiac myocytes.
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