There is little overlap between H3K9me2 and H3K27me3 in mouse liver, indicating a unique and essential role of H3K9me2 in epigenetic control of tissue-specific gene expression.
ChIP-Seq studies in mouse liver indicate that recruitment of the early repressive PER CRY complex, recruitment of the late repressive CRY1 complex, and recruitment of the transcriptional activators CBP/p300 to CLOCK BMAL1 are three temporally distinct phases of the molecular cycle.
These five markers were significantly decreased after 8 weeks of CR in mice liver indicating the persistence of lower oxidative damage through species.
Glucokinase expression in the fasted to re-fed transition was markedly induced in Pten+/− mouse livers, 6 indicating increased insulin sensitivity, suggesting basal HGP regulation is under the control of factors besides insulin signaling, such as neural control.
Both short- and long-term post-transplantation human hepatocyte-like cells resided in the mouse host liver indicating parenchymal penetration and most likely functional engraftment.
The control mice developed large black spleens and livers indicating growth in the spleen and metastasis to the liver.
Furthermore, injection of exogenous rmIL-17 significantly exacerbated liver injury, and even abolished the therapeutic effect of BMSCs transplantation on CCl4-induced mouse liver injury, indicating down-regulating IL-17 is a key for BMSCs-mediated amelioration of hepatic injury in mice.
The pesticides mentioned lead to increased hydroxylation of testosterone in the (mouse) liver, as indicated by increased testosterone hydroxylase activity.
Preneoplastic lesions in the mouse liver are indicated by an abnormal deficiency in glucose-6-phosphatase (14).
Like the rhythmic hepatic transcriptome, mass spectrometry-based analysis of the mouse liver proteome indicates that up to 20% of all hepatic proteins are subject to rhythmic control.
