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A second major set of altered gene functional networks in aging mouse liver involves the interconnected cellular proliferation and death networks.
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This has been explained by CAR-dependent repression of mouse liver gluconeogenesis through a mechanism involving HNF4α and FoxO1 [ 9- 12].
Increased RBP4 impairs insulin signaling in muscle and increases gluconeogenesis in mouse liver, suggesting that RBP4 is involved in the pathogenesis of insulin resistance and is a marker of insulin resistance in mice.
In particular, it is thought that aberrant DNA methylation is central to the development of liver cancers (Goodman and Watson 2002) and is an epigenetic mechanism that underlines the aberrant expression of genes involved in mouse liver carcinogenesis (Counts et al. 1997).
We illustrate this point in our third application involving female and male mouse liver data, in which we analyze the relationship between consensus modules and clinical traits.
Nr4a1 is a known transcriptional regulator of genes involved in glucose metabolism in mouse liver [ 26].
Differentially expressed genes involved in cholesterol homeostasis in mouse liver after TCPOBOP treatment or cholesterol diet as detected by the Steroltalk microarray.
Additionally, we applied our clustered alignment approach to a dataset involving a conditional Mop3 knockout in mouse liver.
Liu has recently shown that MYC is involved in the carcinogenic response of mouse liver to arsenic, another toxic metal [ 39].
The reduced expression of genes involved in cholesterol biosynthesis in the mouse liver suggests a possible role of OPP in reducing atherosclerosis and hence, cardiovascular disease.
Differentially expressed genes involved in glucose and triglyceride metabolism in mouse liver after TCPOBOP treatment or cholesterol diet as detected by the Steroltalk microarray.
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