Sustained CHK2 activity, but not ATM activity, is critical to maintain a G1 arrest after DNA damage in untransformed cells.

Iraia García-SantistebanAlba LlopisLenno KrenningJon Vallejo-RodríguezBram van den BroekAna M ZubiagaRené H Medema

Published in: BMC biology (2021)

Our data indicate that G1 checkpoint maintenance relies on CHK2 and that its negative regulation is crucial for G1 checkpoint recovery after DSB induction.

Keyphrases

dna damage
dna repair
oxidative stress
induced apoptosis
cell cycle
dna damage response
cell cycle arrest
electronic health record
big data
endoplasmic reticulum stress
signaling pathway
artificial intelligence