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. 2012 Mar 1;8(3):e1002566. doi: 10.1371/journal.ppat.1002566

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Cai et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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In the KSHV latently infected cells, LANA upregulates Aurora A expression through targeting Sp1-binding site. The elevated Aurora A induced phosphorylation of p53 on Ser 215 and Ser315 which enhanced the binding affinity of p53 with LANA and promoted LANA^SOCS-mediated ubiquitylation and degradation of p53, and thus inhibited p53 transcriptional and apoptotic activities. Loss of p53 function and aberrant expression of Aurora A trigger chromosome instability for cell survival and growth.