The proline rich domain of p53 is dispensable for MGMT-dependent DNA repair and cell survival following alkylation damage.
Ontology highlight
ABSTRACT: In addition to promoting cell death and senescence, p53 also has important cellular survival functions. A mutant p53, lacking a proline-rich domain (p53ΔP), that is deficient in controlling both cell death and cell cycle arrest, was employed to determine the biological means by which p53 mediates survival upon DNA damage. While p53ΔP and p53-/- cells were equally resistant to many DNA damaging agents, p53ΔP cells showed an exquisite resistance to high doses of the alkylating agent Diazald (N-Methyl-N-(p-tolylsulfonyl)nitrosamide), as compared to cells completely deficient for p53 function. We determined that p53ΔP was capable of transcribing the repair gene, MGMT (O6-methylguanine-DNA methyltransferase) after irradiation or alkylation
SUBMITTER: Baran K
PROVIDER: S-EPMC5635218 | biostudies-literature | 2017 Nov
REPOSITORIES: biostudies-literature
ACCESS DATA