Sentence examples for mouse cells show from inspiring English sources

Mouse cells show a similar inverse correlation between DNA methylation and miR-200c expression.

Also, it remains unclear whether mouse cells show efficient reprogramming of lamin A during iPS induction to become silenced, like ES cells.

SIRT6 knockdown human fibroblasts and SIRT6 deficient mouse cells show H3K9 hyperacetylation at telomeric loci, thereby, demonstrating SIRT6 H3K9 deacetylase targets telomeres [ 47].

Mice that lack PDS5B have multiple developmental anomalies that resemble those found in humans with CdLS and die shortly after birth, 25 whereas Pds5B−/− mouse cells show no defects in sister chromatid cohesion.

After transformation, human and mouse cells show increased expression of secreted CLU at the expense of the intracellular precursor, corroborating the hypothesis that secreted CLU is oncogenic, whereas intracellular CLU is tumour suppressive.

Ser1 phosphorylation is also seen during spermatogenesis in D. melanogaster and in mouse cells, showing evolutionary conservation of this site (62).

Duodenal mouse cells showed considerable expression of this glycan-binding protein (0.8  μg/mg protein or 3  μg/g wet intestinal tissue).

It is interesting to note that while PI3Kβ−/− and PLCγ2−/− mice had similar increases in trabecular bone mass, PLCγ2−/− mouse cells showed a much more robust in vitro osteoclast developmental defect than PI3Kβ−/− mouse cells.

In contrast, growth in mouse cells showed a significant (P<0.05) increase in viral growth compared to wt, where mutation D125G enhanced growth 102-fold, followed by the double and M124I mutants, with 41- and 2-fold increased yields respectively.

In the case of mfn-1 or mfn-2 knockout mice, cells show severe mitochondrial fragmentation (Chen et al, 2003, 2005).

Rad54 knockout mice cells show little or no reduction in spontaneous SCE, but there is a noticeable deficiency in MMC-induced SCE [ 28, 29].