When this interface is disrupted, we note loss of stable dimer-dimer complex formation on the DNA, compromised <i>oriP</i>-containing plasmid replication in cells, and impaired recruitment of the MCM3 complex to the <i>oriP</i> Surface conservation analysis reveals that these residues are part of a larger conserved surface that may be critical for recruitment of replication machinery to the <i>oriP</i> Our results reveal a new region of EBNA1 critical for its activity and one that may be exploited by targeted small molecules to treat EBV-associated disease.<b>IMPORTANCE</b> Epstein-Barr virus (EBV) is a causative agent of various malignancies and may also contribute to autoimmune disease.
The Cancer Genome Atlas data mining in the University of Alabama interactive web resource for pathways associated with poor survival of patients with adrenocortical carcinoma revealed significant upregulation of genes involved in DNA damage and regulation of cell-cycle pathways, such as AURKA, AURKB, CDK1, CDK4, CDK6, PLK1, CHEK1, CHEK2, CDC7, BUB3, and MCM3 (P < .001-.05).
Our study indicates that determination of MCM3 expression level will facilitate the assessment of many different human malignancies in tumor diagnosis, and MCM3 is involved in multiple types of human carcino-genesis.