The Epstein-Barr virus (EBV) infects most of the human population and persists in B-lymphocytes for the lifetime of the host. During the establishment of latent infection a unique repertoire of genes are expressed. The EBV nuclear antigen EBNA3C is essential for growth transformation of primary B-lymphocytes in vitro. EBNA3C regulates the transcription of a number of viral and cellular genes important for the immortalization process. Interaction of EBNA3C with the cellular transcription factor RBP-Jkappa and HDAC1 modulates transcriptional activation. Additionally, EBNA3C disrupts the cyclin/cdk-Rb-E2F pathway that regulates cell cycle progression through the restriction point at G1. Recent studies showed that the carboxy terminal region of EBNA3C from aa 366-992, essential for the immortalization of primary B-cells, interacts with Prothymosin(alpha) (ProTalpha) and Nm23-H1. The interaction of EBNA3C with ProTalpha as well as the histone acetylase p300 suggested a possible role in modulation of histone acetylation and chromatin remodeling. Cell migration assays geared towards determining the effect of EBNA3C on Nm23-H1 antimetastatic function suggests that EBNA3C suppresses the effects of NM23-H1 on the motility of breast carcinoma as well as Burkitt's lymphoma cells. This observation suggests that EBNA3C may be involved in driving the metastatic process in EBV associated human malignancies.
No takes yet. Share an insight, caveat, or question.
Chitra Subramanian (2002) studied this question.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: