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These observations were further confirmed by the mouse senescence model.
Recently, HDAC inhibitors were shown to improve DNA repair in an oncogene-induced senescence model by causing chromatin relaxation [ 55].
Thus, an inverse correlation could be drawn between Mof function, DNA repair and premature senescence (Model summarized in Figure 2).
NF-κB signaling was responsible for establishing SASP in a senescence model of IMR-90 (human skin) fibroblasts expressing H-RasV12 [ 16].
In a replicative senescence model employing human dermal fibroblasts (HDF), G0S2 expression was upregulated in old HDF cells, which suggests that it participates in senescence.
To investigate oxidative stress-induced senescence, we first established a H2O2-induced senescence model for the mouse fibroblast cell line NIH3T3.
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Comparisons between alternative senescence models (Table 3) yielded the following conclusions.
Senescence modeling in natural populations requires modifications to the above methods because one must account for individuals whose date of senescent death is not known.
The experiments were performed on different cell types and were divided into two different groups: premature senescence induced by oxidative stress and other senescence models.
Concerning human aging, many questions about molecular mechanisms have been addressed using in vitro senescence models derived from normal human cells.
As a result 484 genes associated with oxidative stress-induced senescence, 1087 genes associated with other senescence models, and 155 genes which seem to play a role in both experimental settings were determined [ 28].
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