DNA damage during S-phase mediates the proliferation-quiescence decision in the subsequent G1 via p21 expression

• Published in: Nature communications Vol. 8; no. 1; pp. 14728 - 17
• Main Authors: Barr, Alexis R., Cooper, Samuel, Heldt, Frank S., Butera, Francesca, Stoy, Henriette, Mansfeld, Jörg, Novák, Béla, Bakal, Chris
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 20.03.2017; Nature Publishing Group; Nature Portfolio
• Subjects: 13/106; 13/109; 13/89; 14/19; 14/63; 38/35; 631/114/2397; 631/337/1427; 631/80/641/2350; 96/31; Cell cycle; Cell Cycle Checkpoints - genetics; Cell Division - genetics; Cell Line; Cell Proliferation - genetics; Cell Tracking - methods; Cyclin-Dependent Kinase Inhibitor p21 - genetics; Cyclin-Dependent Kinase Inhibitor p21 - metabolism; Cyclin-dependent kinases; Deoxyribonucleic acid; DNA; DNA Damage; G1 Phase - genetics; Gene Knockout Techniques; Genomic Instability; Green Fluorescent Proteins - genetics; Green Fluorescent Proteins - metabolism; Humanities and Social Sciences; Humans; Ionizing radiation; Kinases; Microscopy, Confocal; multidisciplinary; Proteins; S Phase - genetics; Science; Science (multidisciplinary); Tumor Suppressor Protein p53 - genetics; Tumor Suppressor Protein p53 - metabolism; United Kingdom > UK

Following DNA damage caused by exogenous sources, such as ionizing radiation, the tumour suppressor p53 mediates cell cycle arrest via expression of the CDK inhibitor, p21. However, the role of p21 in maintaining genomic stability in the absence of exogenous DNA-damaging agents is unclear. Here, usi...