作者: T I Kuschak , B C Kuschak , C L Taylor , J A Wright , F Wiener
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摘要: The mechanisms through which the oncoprotein c-Myc initiates locus-specific gene amplification are not understood. When analysing initiation mechanism of c-Myc-dependent mouse ribonucleotide reductase R2 (R2) gene, we observe illegitimate DNA replication gene. We demonstrate multiple simultaneous c-Myc-induced forks, whereas normally replicates with a single fork. In contrast, cyclin C only fork irrespective deregulation. addition to de novo also bi-allelic R2, abrogating its normal mono-allelic pattern. Moreover, several chromosomal regions display profiles. Thus, can act as an replication-licensing factor that promotes and timing adversely impacts upon genomic stability.