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- W2326663831 abstract "See related article, pp 866–877 Calcineurin is protein phosphatase with characteristic calcium- and calmodulin-dependent activation through its regulatory subunits.1 Activated calcineurin dephosphorylates downstream transcription factor nuclear factor of activated T cells (NFAT), which leads to its nuclear translocation and transcriptional activation.1 Calcineurin-NFAT signaling axis is initially discovered as an essential pathway for T-cell activation1 but has now been implicated in a broad range of cellular processes and cell types ranging from fungus to plants. In the heart, calcineurin-mediated signaling is recognized as a common intracellular pathway leading to cardiac hypertrophy and pathological remodeling triggered by a plethora of pathological stressors.2 In this issue, Zhu et al3 add a new piece of evidence to a significant body of literature4 and further demonstrate that genetic or pharmacological attenuation of calcineurin signaling can have a significant ameliorative effect on the pathogenesis of cardiac hypertrophy and dysfunction in response to various stresses.Like many stress-induced signaling pathways, calcineurin pathway is also tightly controlled by a cohort of endogenous negative regulators in cells.5 The prototypic regulator of calcinurin-1 (RCAN1, also known as ADAPT78, CSP1, DSC1, DSCR1, MCIP1, RCN1, and calcipressin1) is transcriptionally controlled by NFAT and serves as a key negative feedback …" @default.
- W2326663831 created "2016-06-24" @default.
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- W2326663831 date "2016-05-01" @default.
- W2326663831 modified "2023-09-24" @default.
- W2326663831 title "Positive Role for a Negative Calcineurin Regulator in Cardiac Hypertrophy" @default.
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- W2326663831 doi "https://doi.org/10.1161/hypertensionaha.116.07140" @default.
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