Cell cycle arrest in response to a double-stranded break is initially maintained by the DNA damage checkpoint and later by the spindle assembly checkpoint.

The localization of Rad53 cell cycle checkpoint kinase to many gene promoters and the dynamic changes in response to replication stress suggests that the kinase may coordinate genome stability and gene expression.

The S-phase checkpoint has roles in all phases of the cell cycle, which has implications for the majority of cancers that lack cell cycle controls.

The combination of statistical inference and perturbation experiments reveals that trans-generational inheritance of cell size and cell-cycle speed, coupled through a minimum-size checkpoint, shapes paradoxical cell-cycle correlations in lineage trees.

The initiation of DNA damage checkpoint recovery involves ATM-mediated E3 ubiquitin ligase E6AP phosphorylation which disrupts E6AP-MASTL association and leads to MASTL protein accumulation and cell cycle resumption.

Activation of a DNA-damage cell cycle checkpoint during aging causes genome instability and senescence in yeast mother cells.

Evolutionary adaptation to a constitutive perturbation of DNA replication reveals that adaptive mutations in three conserved pathways interact to restore faithful chromosome replication and segregation.

Anti-tumor properties of sub-class of xanthine analogs involve restoration of p53 pathway transcriptome, independent of p53/p73, dependent on ATF3/ATF4 and Noxa in mutated-p53 tumors and the compounds trigger an S-phase checkpoint.

Experimental manipulation of a core DNA damage response factor and cell-cycle checkpoint regulators reveals a key role for these processes in the progenitor cells that fuel limb regeneration.

During tumorigenesis loss of p53 not only abrogates cell cycle arrest and apoptosis, but also suppresses the induction of replication-stress-induced DNA double-stranded breaks.