EBNA3A contributes to the regulation of <i>p16<sup>INK4A</sup></i>.

<p>(<b>A</b>) Western blot analysis of three LCLs established with virus derived from B95.8-EBV BAC (WT) and two established with EBNA3A-KO recombinants. The steady state levels of p16<sup>INK4A</sup> (p16) are elevated in the EBNA3A-KO cells relative to the WT-EBV infected cells. It should be noted that similar results were reported using a larger panel of EBNA3A-KO LCLs <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1000951#ppat.1000951-Hertle1" target="_blank">[8]</a>. An LCL 3CHT (3CHT) with (+) or without (-) HT is shown for comparison. (<b>B</b>) <b>&</b> (<b>C</b>) ChIP analysis of H3K27me3 and H3K4me3 distribution on exon 1 (site C) and site A in the <i>p16<sup>INK4A</sup>-ARF</i> locus from an EBNA3A-KO LCL (3AKO) and a WT-EBV LCL (WT).</p>