Sentence examples for models mutations in from inspiring English sources

In murine models, mutations in the Dnmt3b gene negatively affect proper embryonic development [2], [5].

In murine models, mutations in the clock gene were first associated with glucose homeostasis [ 32] and later with obesity, hyperglycemia and hyperinsulinemia [ 33].

Based on structural models, mutations in PYR1 and ΔNABI1D413L of ABAleon2.1 were selected that potentially reduce but not abolish PYR1-ΔNABI1D413L interaction (Melcher et al., 2009; Miyazono et al., 2009; Mosquna et al., 2011; Zhang et al., 2012) resulting in the new constructs ABAleon2.11 ABAleon2.17.

In fact, both in human and mouse models, mutations in p53 do not account per se for the accumulation of the protein and it is well established that high expression of p53MUT is mostly found in advanced cancers (Goh et al, 2011).

Using a plant model, mutations in animal pathogenic bacteria can easily be screened for putative virulence factors, a process which if done using existing animal infection models would be time-consuming and tedious.

Consequently, according to our model, mutations in PS1 that prevent processing, such as those shown in Figure 1, C410Y and Δe9, will decrease the activity of the β-catenin·Tcf-4 complex but will not affect, or even up-regulate, other pathways involving CBP, such as those related to CREB, NF-κB or p53 [59], [60], [60].

Based on this model mutations in either PC1 or PC2 can disrupt these pathways leading to abnormal cell proliferation [ 17].

Like those seen in the Sander et al 59 mouse model, mutations in BL samples were also identified within the TCF3 target gene cyclin D3.

The study of model mutations in the carboxyl-terminus of FIX is particularly informative to elucidate the interplay between pathogenic molecular mechanisms impairing protein biosynthesis and function.

In addition, modeling mutations in three dimensions (if a crystal structure of the target has been solved) would allow approved drugs to be readily screened in silico against the mutant and normal targets.

In support of this model, mutations in the LN domains of the α1 and α2 chains compromise laminin function in vivo (Xu et al, 1994; Patton et al, 2008; Edwards et al, 2010).