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We also highlighted that Hey2 is involved in radiation-induced EndoMT and that Hey2 invalidation reduces EndoMT and tissue damage.
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Data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation.
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Hey proteins mechanistically repress target genes via histone deacetylase recruitment and histone deacetylation.
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Results suggest that bone morphogenetic protein signaling plays pivotal roles in retinal progenitor cell differentiation into late differentiating retinal cell types and in Muller glia maturation; these effects were mediated, at least in part, by Hey2
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Hey1 and Hey2 in endothelial cells play important roles in vascular development.
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findings indicate that Hey1 and Hey2 control the spatial and temporal pattern of auditory HC differentiation.
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CHF1/Hey2 may contribute to Brugada syndrome.
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Common variants at SCN5A-SCN10A and HEY2 are associated with Brugada syndrome, a rare disease with high risk of sudden cardiac death.
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Data indicate that Hairy and Enhancer of Split-related with YRPW motif (HEY)2 decreases skeletal mass and regulates bone remodeling in male mice.
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Data indicate that Notch1 and Notch2 are expressed and localized in the nuclei of the label-retaining cells (LRCs), and the expression of Notch-inducible genes, Hes1 and Hey2, was elevated in LRCs.
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Survivor mice lacking the Hesr2 gene exhibit fibrosis in the aortic valve and ventricle in adulthood, thus suggesting that Hesr2 plays an important role in maintaining the homeostasis of the aortic valve and ventricle.
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Transcription factor CHF1/Hey2 regulates EC coupling and heart failure in mice through regulation of FKBP12.6.
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These findings support the hypothesis that CHF1/Hey2 is an important regulator of MMP10 expression.
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Hey2 regulates the later steps of coronary vascular development in both a myocardial-dependent, non-cell autonomous fashion and likely a vascular cell-specific effect as well.
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CHF1/Hey2 expression levels influence hypertrophy and the progression to heart failure in response to pressure overload through modulation of apoptosis and GATA4 activity.
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Data demonstrate that CHF1/Hey2 promotes physiological over pathological hypertrophy through suppression of apoptosis and regulation of multiple transcriptional pathways.
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Hey2 loss does not affect aortic development, but it instead leads to a massive postnatal cardiac hypertrophy with high lethality during the first 10 days of life.
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Homozygotes for the Hey2 mutant allele display a spectrum of cardiac malformations including ventricular septal defects, tetralogy of Fallot, and tricuspid atresia.
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CHF1 plays an important role in regulation of ventricular septation in mammalian heart development and is important for normal myocardial contractility.
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results indicate that hairy enhancer of split related with YRPW motif 1 and 2 negatively regulate neuronal basic helix- loop-helix genes, promote maintenance of neural precursor cells, and increase late-born cell types in the developing brain
