A recent study has documented MEIS genomic occupancy in the branchial arches (Amin et al., 2015), enabling us to compare on a genome-wide basis the loci binding MEIS in the AHF with those binding Nkx2-5 in the heart.
These results indicate that MEIS1 binding on the Popdc2 enhancer predominates in the AHF, while NKX2-5 binding predominates in the heart.
We evaluated m2AChR binding only in the heart because these receptors are sparse in the liver and cerebellum.
As well as these glucoregulatory effects, GLP-1 also has binding sites in the heart, and clinical studies demonstrating the cardioprotective properties of incretin-modulating agents are continuing to emerge [ 10– 16].
Since ChIP-Seq analysis of SIRT1 genome-wide binding in the mouse heart identified several promoters of genes involved in the immune function, and transcriptomic analysis pointed to an upregulation of 8 key genes implicated in the immune response, we sought to quantify accurately the white blood cell (WBC, leukocytes) number in the peripheral blood of WT and mIGF-1 Tg mice.
Similar desensitizing effects of stress on α1-receptors were reported in the peripheral nervous system, where chronic stress reduced the α1-stimulated contraction of the isolated vas deferens (Singh et al, 2001) and downregulated the density of α1-binding sites in the heart (Torda et al, 1985).
To assess whether the NKX2-5-binding loci are likely to identify transcriptional enhancer regions, we compared them with those enriched for binding of P300 in the heart at the same stage (Blow et al., 2010).
Transgenic overexpression of the Ca2+-binding protein S100A1 in the heart leads to increased in vivo myocardial contractile performance.
Here, we show that loss of an MT-binding protein, CENP-F, in the heart results in dilated cardiomyopathy.
In view of the fact that we found SIRT1 localized in 22 to 28% of cardiomyocytes nuclei, with the aim of understanding the nuclear genomic function of this deacetylase, we performed genome-wide profiling of its binding to DNA in the hearts of WT or mIGF-1 Tg mice by using ChIP-Seq and a specific ChIP-grade commercial antibody.
