| http://purl.uniprot.org/citations/17409144 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17409144 | http://www.w3.org/2000/01/rdf-schema#comment | "Epstein-Barr virus (EBV) infects most of the human population and persists in B lymphocytes for the lifetime of the host. The establishment of latent infection by EBV requires the expression of a unique repertoire of genes. The product of one of these viral genes, the EBV nuclear antigen 3C (EBNA3C), is essential for the growth transformation of primary B lymphocytes in vitro and can regulate the transcription of a number of viral and cellular genes important for the immortalization process. This study demonstrates an associated function of EBNA3C which involves the disruption of the G2/M cell cycle checkpoint. We show that EBNA3C-expressing lymphoblastoid cell lines treated with the drug nocodazole, which is known to block cells at the G2/M transition, did not show a G2/M-specific checkpoint arrest. Analyses of the cell cycles of cells expressing EBNA3C demonstrated that the expression of this essential EBV nuclear antigen is capable of releasing the G2/M checkpoint arrest induced by nocodazole. This G2/M arrest in response to nocodazole was also abolished by caffeine, suggesting an involvement of the ATM/ATR signaling pathway in the regulation of this cell cycle checkpoint. Importantly, we show that the direct interaction of EBNA3C with Chk2, the ATM/ATR signaling effector, is responsible for the release of this nocodazole-induced G2/M arrest and that this interaction leads to the serine 216 phosphorylation of Cdc25c, which is sequestered in the cytoplasm by 14-3-3. Overall, our data suggest that EBNA3C can directly regulate the G2/M component of the host cell cycle machinery, allowing for the release of the checkpoint block."xsd:string |
| http://purl.uniprot.org/citations/17409144 | http://purl.org/dc/terms/identifier | "doi:10.1128/jvi.00053-07"xsd:string |
| http://purl.uniprot.org/citations/17409144 | http://purl.uniprot.org/core/author | "Murakami M."xsd:string |
| http://purl.uniprot.org/citations/17409144 | http://purl.uniprot.org/core/author | "Choudhuri T."xsd:string |
| http://purl.uniprot.org/citations/17409144 | http://purl.uniprot.org/core/author | "Lan K."xsd:string |
| http://purl.uniprot.org/citations/17409144 | http://purl.uniprot.org/core/author | "Robertson E.S."xsd:string |
| http://purl.uniprot.org/citations/17409144 | http://purl.uniprot.org/core/author | "Verma S.C."xsd:string |
| http://purl.uniprot.org/citations/17409144 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17409144 | http://purl.uniprot.org/core/name | "J Virol"xsd:string |
| http://purl.uniprot.org/citations/17409144 | http://purl.uniprot.org/core/pages | "6718-6730"xsd:string |
| http://purl.uniprot.org/citations/17409144 | http://purl.uniprot.org/core/title | "The ATM/ATR signaling effector Chk2 is targeted by Epstein-Barr virus nuclear antigen 3C to release the G2/M cell cycle block."xsd:string |
| http://purl.uniprot.org/citations/17409144 | http://purl.uniprot.org/core/volume | "81"xsd:string |
| http://purl.uniprot.org/citations/17409144 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17409144 |
| http://purl.uniprot.org/citations/17409144 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/17409144 |
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| http://purl.uniprot.org/uniprot/#_A0A4P8PR71-mappedCitation-17409144 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17409144 |
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