Replicatively senescent cells are arrested in G1 and G2 phases - Figure F1

Senescent human fibroblast cultures contain a large fraction of putative G2-arrested cells with 4N DNA content. (A) Propidium iodide (PI) staining and flow cyctometric analysis of HCA2 normal human foreskin fibroblasts. Cells entered senescence at PD73. (B) PI staining of replicatively senescent human lung fibroblasts WI-38, and IMR-90 at PDs 73 and 68 respectively. (C) The fraction of 4N cells in senescent cell population does not diminish with time. Replicatively senescent HCA2 cells were analyzed by PI staining at weekly intervals for 10 weeks stating from the onset of senescence.

PDF) Possibility of inducing tumor cell senescence during therapy

Cellular Senescence: From Mechanisms to Current Biomarkers and

Full article: Dysregulated endolysosomal trafficking in cells

The molecular architecture of cell cycle arrest

Full article: Senescence from G2 arrest, revisited

Necessary and Sufficient Role for a Mitosis Skip in Senescence

Key elements of cellular senescence involve transcriptional

Reduced transcriptional activity in the p53 pathway of senescent

Reorganization of chromosome architecture in replicative cellular

Cell cycle shift from G0/G1 to S and G2/M phases is responsible

Cell cycle re-entry and arrest in G2/M phase induces senescence

Cell cycle re-entry and arrest in G2/M phase induces senescence

FGF19 induces the cell cycle arrest at G2-phase in chondrocytes

Global spliceosome activity regulates entry into cellular

Cellular senescence: the good, the bad and the unknown