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Epstein-Barr nuclear antigen 1

UniProtKB accession:  P03211
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Go to UniProtKB:  P03211
UniProtKB description:  Responsible for the origin of replication (oriP) dependent replication and maintenance of viral episomes during latent infection (PubMed:2996781, PubMed:15479791). EBNA1 dimer interacts with the DS (dyad symmetry) element within the origin of replication oriP and with a host mitotic chromosome to initiate viral DNA replication during latency (PubMed:2996781, PubMed:8551585, PubMed:24067969, PubMed:31142669). EBNA1 binding to DS recruits the host origin recognition complex (ORC) (PubMed:12953058). Governs the faithful mitotic segregation of the viral episomes by binding both the FR (family of repeats) element within oriP and the host mitotic chromosomes (PubMed:15479791, PubMed:11172042, PubMed:24067969). Forms a cell cycle-dependent tyrosine-dependent DNA cross-link and single-strand cleavage at oriP required for terminating replication and maintaining viral episomes (PubMed:33482082). Counteracts the stabilization of host p53/TP53 by host USP7, thereby decreasing apoptosis and increasing host cell survival (PubMed:15808506). Induces degradation of host PML through the ubiquitin-proteasome system, which promotes lytic reactivation and may impair the host cell DNA repair (PubMed:18833293). Increases the association of CK2 with PML proteins which increases the phosphorylation of PML proteins by CK2, triggering the polyubiquitylation and degradation of PML (PubMed:20719947). Displays inhibitory effects on a SUMO2-modified complex that includes STUB1, KAP1 and USP7 (PubMed:32176739). This inhibitory effect possibly participates to the maintenance of latency linked to PML silencing (PubMed:32176739).
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