ATM and ATR are key effectors of the cellular response to DNA damage, instructing a damaged cell to halt cell cycle progression and either initiate DNA repair processes or programmed cell death. While much research has focused on the identification of moleculaes that help transduce these signals throughout the cell, in their current paper, Dr. Lawrence Donehower and colleagues address the issue of how a cell returns to normal after DNA damage is successfully repaired.
Dr. Donehower and colleagues show that the phosphatase PPM1D effectively curtails the DNA damage checkpoint response by dephosphorylating the ATM/ATR targets, Chk1 and p53 – enabling the cell to resume a homeostatic state. "From my point of view, the most interesting thing about this study is a new insight on p53 regulation…those tumors that show amplified and overexpressed PPM1D may be analogous to those tumors with amplified and overexpressed MDM2. In both tumor types, p53 may be functionally inactivated and this promotes tumorigenesis," explains Dr. Donehower.
Heather Cosel | EurekAlert!
A Map of the Cell’s Power Station
18.08.2017 | Albert-Ludwigs-Universität Freiburg im Breisgau
On the way to developing a new active ingredient against chronic infections
18.08.2017 | Deutsches Zentrum für Infektionsforschung
16.08.2017 | Event News
04.08.2017 | Event News
26.07.2017 | Event News
18.08.2017 | Life Sciences
18.08.2017 | Physics and Astronomy
18.08.2017 | Materials Sciences