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The purpose of this review is to discuss the evidence that various dietary bioactive compounds can modulate cellular senescence in vitro and to summarize findings and mechanisms that might be useful for the development of health-promoting nutraceuticals.
Interestingly however, repression of PTEN by miR-17 was not found to be sufficient to modulate cellular senescence.
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The involvement of SIRT1 in modulating cellular senescence was identified with its deacetylation of p53 and eventual attenuation of promyelocytic leukemia protein (PML -mediated PML -mediatedlular senescence (Langley et al., 2002).
In Saccharomyces cerevisiae, silent information regulator 2 (Sir2) modulates cellular senescence.
Among them are the genes modulating cellular senescence, DNA repair, oxidative stress, longevity, angiogenesis, differentiation, glycolysis, tumor motility and invasion, and even bone remodeling [1,2].
While premature senescence can be induced by a plethora of cell-extrinsic and cell-intrinsic stressors, little is known about the possible role of autophagy in modulating injury-induced cellular senescence in vivo.
In continuation of these studies we initiated to assess whether these agents can modulate the induction of premature cellular senescence.
In aging Drosophila, abnormal apoptotic events have been observed in muscle and fat tissue [ 8], but the extent to which apoptosis (or cellular senescence) might modulate Drosophila life span remains largely unknown.
Misexpression of Polycomb repressive complex 1 (PRcomponentsents in human cells profoundly influences the onset of cellular senescence by modulating transcription of the INK4a tumor suppressor gene.
Thus, IGF-1 can promote premature cellular senescence by modulating the SIRT1-p53 axis.
This conclusion is consistent with previous findings that PPAR γ regulates cellular senescence by modulating p16 expression in the old fibroblasts.
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