PKR is not a universal target of tumor suppressor p53 in response to genotoxic stress.
It has been recently reported that p53 activation can lead to the induction of PKR-eIF2alpha phosphorylation pathway. However, we demonstrate that PKR and eIF2alpha phosphorylation at serine 51 are not downstream of p53 in response to doxorubicin treatment suggesting that PKR is not a universal target of p53 as proposed.
Rahman
Mashrur
M
Lady Davis Institute for Medical Research, McGill University, Sir Mortimer B. Davis-Jewish General Hospital, Montreal, QC Canada.
Lem
Christopher
C
Muaddi
Hala
H
Koromilas
Antonis E
AE
D000818:Animals; D015179:Colorectal Neoplasms / Q000188:drug therapy / Q000378:metabolism*; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000819:agonists / Q000378:metabolism*; D004249:DNA Damage; D004317:Doxorubicin / Q000494:pharmacology / Q000627:therapeutic use; D015852:Eukaryotic Initiation Factor-2 / Q000819:agonists / Q000378:metabolism*; D006801:Humans; D051379:Mice; D010766:Phosphorylation / Q000187:drug effects / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000819:agonists / Q000235:genetics / Q000378:metabolism*; D023041:Xenograft Model Antitumor Assays; D019892:eIF-2 Kinase / Q000187:drug effects / Q000378:metabolism*
D050759:Cyclin-Dependent Kinase Inhibitor p21; D015852:Eukaryotic Initiation Factor-2; D016159:Tumor Suppressor Protein p53; D004317:Doxorubicin; D019892:eIF-2 Kinase