{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Saha A"],"funding":["NCI NIH HHS"],"pagination":["e1002573"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3305458"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(3)"],"pubmed_abstract":["EBV latent antigen EBNA3C is indispensible for in vitro B-cell immortalization resulting in continuously proliferating lymphoblastoid cell lines (LCLs). EBNA3C was previously shown to target pRb for ubiquitin-proteasome mediated degradation, which facilitates G1 to S transition controlled by the major transcriptional activator E2F1. E2F1 also plays a pivotal role in regulating DNA damage induced apoptosis through both p53-dependent and -independent pathways. In this study, we demonstrate that in response to DNA damage LCLs knocked down for EBNA3C undergo a drastic induction of apoptosis, as a possible consequence of both p53- and E2F1-mediated activities. Importantly, EBNA3C was previously shown to suppress p53-induced apoptosis. Now, we also show that EBNA3C efficiently blocks E2F1-mediat"],"journal":["PLoS pathogens"],"pubmed_title":["E2F1 mediated apoptosis induced by the DNA damage response is blocked by EBV nuclear antigen 3C in lymphoblastoid cells."],"pmcid":["PMC3305458"],"funding_grant_id":["CA137894-02","R01 CA138434","R01 CA137894","CA138434-02"],"pubmed_authors":["Saha A","Morizur L","Upadhyay SK","Lu J","Robertson ES","Aj MP"],"additional_accession":[]},"is_claimable":false,"name":"E2F1 mediated apoptosis induced by the DNA damage response is blocked by EBV nuclear antigen 3C in lymphoblastoid cells.","description":"EBV latent antigen EBNA3C is indispensible for in vitro B-cell immortalization resulting in continuously proliferating lymphoblastoid cell lines (LCLs). EBNA3C was previously shown to target pRb for ubiquitin-proteasome mediated degradation, which facilitates G1 to S transition controlled by the major transcriptional activator E2F1. E2F1 also plays a pivotal role in regulating DNA damage induced apoptosis through both p53-dependent and -independent pathways. In this study, we demonstrate that in response to DNA damage LCLs knocked down for EBNA3C undergo a drastic induction of apoptosis, as a possible consequence of both p53- and E2F1-mediated activities. Importantly, EBNA3C was previously shown to suppress p53-induced apoptosis. Now, we also show that EBNA3C efficiently blocks E2F1-mediat","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012","modification":"2025-04-22T06:58:31.732Z","creation":"2019-03-27T00:51:13Z"},"accession":"S-EPMC3305458","cross_references":{"pubmed":["22438805"],"doi":["10.1371/journal.ppat.1002573"]}}