ATR disruption leads to chromosomal fragmentation and early embryonic lethality
AUTOR(ES)
Brown, Eric J.
FONTE
Cold Spring Harbor Laboratory Press
RESUMO
Although a small decrease in survival and increase in tumor incidence was observed in ATR+/− mice, ATR−/− embryos die early in development, subsequent to the blastocyst stage and prior to 7.5 days p.c. In culture, ATR−/− blastocysts cells continue to cycle into mitosis for 2 days but subsequently fail to expand and die of caspase-dependent apoptosis. Importantly, caspase-independent chromosome breaks are observed in ATR−/− cells prior to widespread apoptosis, implying that apoptosis is caused by a loss of genomic integrity. These data show that ATR is essential for early embryonic development and must function in processes other than regulation of p53.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=316378Documentos Relacionados
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