Sentence examples for proliferation as a consequence of from inspiring English sources

72, 74– 76 Suppression of cancer cell proliferation as a consequence of SIRT1 downregulation might be attributable to telomere dysfunction and increased acetylation and subsequent activation of p53.

All together, these observations are consistent with a phenotype of checkpoint-guided inhibition of cell proliferation as a consequence of oncogene-induced growth arrest.

Cell cycle progression is an important regulatory mechanism for cell proliferation, as dysregulation of the cell cycle results in unrestrained cell proliferation as a consequence of tumorigenesis [ 6].

Consistent with our in vitro results, in vivo metformin administration inhibited ESCC cell growth through the integrative effects of apoptosis, autophagy and cell proliferation as a consequence of metformin-mediated inactivation of Stat3/Bcl-2 pathway.

We postulated that the DNA damage observed in the E6.5 embryos led to p53 activation and reduced cellular proliferation as a consequence of cyclin G1 and p21-mediated cell-cycle arrest (Cazzalini et al., 2010; Kimura et al., 2001).

Interestingly, our results also show that the anti-apoptotic activity of estradiol is preserved in breast cancer cells that do not require estradiol for proliferation as a consequence of prolonged estrogen deprivation.

In similar experiments that allowed comparison of the BrdU and biotin techniques for proliferation analysis of candidate HSC we observed significant changes in proliferation rates as a consequence of high dose long term BrdU administration (Fig. S2).

This result was anticipated by our previous observation that genetic disruption of Dictyostelium Rb function does not affect proliferation, presumably as a consequence of the lack of detectable G1 phase in growing Dictyostelium amoebae [10].

However, it has been well described that mitochondrial proliferation can occur as a consequence of mtDNA disease in man.

Indeed, it has been proposed that such IS element proliferations take place as a consequence of the imposition of relaxed selection on a large number of genes (Moran and Plague 2004; Plague et al. 2008), facilitating the expansion of IS elements into genomic space encompassing genes evolving under relaxed selection.

Indeed loss of Cyclin D1 in over-expressing miR-199b-5p clones are a reminder of the similar effects seen in Ccnd1 /– mice, which have decreased early GNP proliferation and early ataxia as a consequence of a delay in acquiring normal cerebellar function, thus affecting progression of the pre-neoplastic lesions to MBs [43].