In addition, loss-of-function experiments in mouse fibroblast demonstrated that SIRT1 is required for replicative senescence resulting from chronic genotoxic stress [ 42].
In vitro studies using mouse embryo fibroblasts demonstrate that inhibition of Aurora-A can have either positive or negative effects on cell growth as a function of p53 status.
Specifically, we have applied sustained and cyclic, radial stretching at large strains to NIH3T3 mouse fibroblasts, and have demonstrated that cell viability, adhesion and morphology were maintained following stretching.
In vitro studies demonstrated that mouse fibroblasts survived and proliferated inside closed porous tubes.
Subsequently, Vierbuchen and colleagues [ 38] demonstrated that mouse fibroblasts, following treatment with lentivirus containing genes for three transcription factors expressed in the nervous system, Ascl1, Brn2, and Myt1l, could be induced to differentiate directly to neurons.
Seminal papers from the Yamanaka group demonstrated that mouse fibroblasts could be reprogrammed to mESC-like cells by the expression of four mESC-specific transcription factor genes (Klf4, c-Myc, Oct-3/4, and Sox2).
After SCNT, another breakthrough in cell fate conversion was achieved in 2006, with the Japanese scientist Yamanaka and his colleagues demonstrated that mouse fibroblasts could be reprogrammed into pluripotent state by exogenous expression of four transcriptional factors, Oct4, Sox2, Klf4 and c-Myc.
Keren-Paz et al. (2006) demonstrated that NIH3T3 mouse fibroblasts overexpressing AzI had elevated ODC and polyamine levels, and proliferated faster than control cells.
DNA transfection experiments using the NIH 3T3 mouse fibroblast cell line have demonstrated that chemically induced tumors and chemically transformed cell lines frequently contain dominant transforming genes.
The indirect cytotoxicity assessments demonstrated the photocrosslinked hydrogels was compatible to mouse fibroblasts (L929 cells), indicating their potential as tissue engineering scaffolds.
