Key result
Endothelin-1 elicits local nuclear envelope Ca2+ release via InsP3R, activating nuclear CaMKII and triggering HDAC5 nuclear export, a pathway distinct from global Ca2+ transients.
Population
Adult ventricular myocytes
Design
Preclinical
Authors
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Does not inform clinical practice; leaves open selective nuclear InsP3R targeting for gene regulation in cardiac disease.
Identifies a distinct, local InsP3-dependent perinuclear Ca2+ signaling pathway that regulates cardiac myocyte gene transcription independently of the global Ca2+ transients used for contraction.
Xu Wu (2006) studied Cardiac hypertrophy signaling. Endothelin-1 (ET-1) was evaluated on HDAC5 phosphorylation and nuclear export. Endothelin-1 elicits local nuclear envelope Ca2+ release via InsP3R, activating nuclear CaMKII and triggering HDAC5 nuclear export, a pathway distinct from global Ca2+ transients.
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