Epstein-Barr virus nuclear antigen 2 induces FcRH5 expression through CBF1.

摘要: Fc-receptor homolog 5 (FcRH5) is a recently identified B-cell membrane protein of unknown function. In Burkitt lymphoma cell lines with chromosome 1q21 abnormalities, FcRH5 expression deregulated, implicating in lymphomagenesis. Epstein-Barr virus infects and immortalizes B cells, implicated the etiology several tumors origin. Overexpression genes located on 1q21-25 has been proposed as surrogate for lymphoma. We now report that nuclear antigen 2 (EBNA2) markedly induces gene, encoded 1q21. Induction occurred absence other viral proteins did not require de novo synthesis. EBNA2 lacks DNA-binding domain can target responsive through host DNA binding CBF1. show induction by strictly CBF1 dependent, it was abolished CBF1-deficient cells. Accordingly, targeted sites present promoter vivo, detected chromatin immunoprecipitation. These results identify novel, direct may contribute to development virus–associated tumors.