Sentence examples for mouse models provided from inspiring English sources

All these mouse models provided fundamental understanding of the essential function of imprinted genes in embryonic development as well as mechanisms of genomic imprinting regulation.

Recent knockout mouse models provided evidence that TH entry into the brain is largely dependent on two TH transporters, monocarboxylate transporter 8 (MCT8) and organic anion-transporting polypeptide 1c1 (OATP1c1) [ 4– 9].

We focused on the behavior of the endodermal enhancers in neonatal liver, and our array of mouse models provided an opportunity to compare wild-type chromosomes with alleles containing a variety of mutations in the CTCF sites.

Studies on genetic mouse models provided experimental evidence that mutation in genes that control chromosome segregation promotes cancer formation by increasing loss of heterozygosity (Baker & van Deursen, 2010), but the effect on carcinogenesis was context dependent and aneuploidy suppressed tumorigenesis in some mouse strains (Weaver et al, 2007; Schvartzman et al, 2010).

The large numbers of mice used in the study, and the variety of different mouse models provided greater sensitivity and statistical confidence in selection of differentially expressed genes allowed us to identify a comprehensive list of genes, PRGs, from our BMAP microarrays that are consistently deregulated in these models.

Our study, together with evidences from C. elegans and mouse models, provides an important cue to WS therapy.

Collectively, these transgenic mouse models provide interesting new insights regarding pathophysiological functions of GSH in the liver.

Genetically engineered BCC mouse models provide one important tool for the study of the biology of human BCCs and for evaluating therapeutic interventions, as these mice produce multiple genetically defined tumors within a relatively short period of time.

Mouse models provide important information regarding pharmacokinetics and in vivo efficacy of novel compounds [15] [17], [54] [57].

However, since Trpc6 is ubiquitously expressed and the reported transient overexpressors do not show any selectivity our mouse models provide novel tools to study the contribution of podocyte dysfunction in the pathogenesis of FSGS.

Mouse models provide an opportunity to study such mechanisms.