Sentence examples for mutant mouse embryos from inspiring English sources

Nodal null mutant mouse embryos do not gastrulate, and hypomorphic mutants form abnormal hearts [16], [17].

To test this, we generated the PTHrP−/−; Catnbc/c; Col2a1-Cre double mutant mouse embryos.

Mouse embryonic fibroblasts (MEF) were isolated from 13.5 day wild-type and Fsp27 mutant mouse embryos as described [43].

Sprouty4 does not oscillate in Hes7-null mutant mouse embryos, and Hes7 can inhibit FGF-induced transcriptional activity of the Sprouty4 promoter.

Detailed genetic analyses suggest that both the transcriptional activator and repressor functions of Gli proteins are compromised in mutant mouse embryos with defective cilia [4], [5], [6], [7].

We found that Hes1 mutant mouse embryos had severe thyroid hypoplasia related to low thyroid progenitor cell numbers, an abnormality that was independent from p57.

Transfecting dsRNA oligonucleotides containing inosine-uracil base pairs into Adar1 mutant mouse embryo fibroblasts reduces the aberrant innate immune response.

These data are consistent with our previous data in Figure 3E showing reduced epithelial proliferation in the double mutant mouse embryo cochlear duct.

Aberrant immune responses in Adar1 mutant mouse embryo fibroblasts are dramatically reduced by restoring the expression of editing-active cytoplasmic ADARs.

Our preliminary data indicate, however, that combining Ifih1 with Adar1 does not rescue the lethality of the Adar1 mutant mouse embryo (data not shown), suggesting that MDA5 is not the sole mediator of the Adar1 mutant phenotype.

Gem induced eIF2 phosphorylation and downstream transcription factors ATF4 and CHOP in PCCs, and these effects occurred in an eIF2 α-S51 phosphorylation-dependent manner as determined using PANC-1 cells, and wild type and S51 mutant mouse embryo fibroblasts.