Gene name: | RRM2B |
Aging type: | Prevent |
Aging characteristic: |
Tissue type: | -- |
Cell name: | IMR-90 |
Experiment: | SA-β-gal activity assay//Western blot |
Description: | Unexpectedly, the silencing of RRM2B triggered premature senescence in young IMR90 cells. The specific silencing of RRM2B led to the progressive accumulation of multiple senescent regulators, including p53, p21CIP1 and p16INK4A, from day 7 to 19. |
Regulatory pathway: | P38 MAPK//P53 |
R-AG-Pathway: | --//-- |
Official symbol(s): | MAKP14//TP53 |
Pathway experiment: | SA-β-gal activity assay//Western blot//BrdU assay |
Pathway description: | p38MAPK phosphorylation was profoundly increased when RRM2B was silenced compared to shRRM2Bmut-expressing cells. Downstream targets of p38MAPK were also activated, as indicated by the significant elevation of phosphorylated MAPKAPK-2, a substrate of p38MAPK, and the phosphorylation of HSP27, a substrate of MAPKAPK-236.Interestingly, the silencing of p53 by shRNA in shRRM2Bexpressing cells was sufficient to rescue premature senescence, as indicated by the significant reduction in SA-β-gal activity and the increase in the replication index .?Cells expressing both shRRM2B and shTP53 showed reduced expression of p21CIP1 and increased levels of RRM1 and RRM2 , whereas p16INK4A was unchanged compared to cells expressing shRRM2B alone. |
Annotation:
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