Evi-2, a common integration site involved in murine myeloid leukemogenesis

Arthur M. Buchberg, Hendrick G. Bedigian, Nancy A. Jenkins, Neal G. Copeland

Research output: Contribution to journalArticle

84 Scopus citations

Abstract

BXH-2 mice have the highest incidence of spontaneous retrovirally induced myeloid leukemia of any known inbred strain and, as such, represent a valuable model system for identifying cellular proto-oncogenes involved in myeloid disease. Chronic murine leukemia viruses often induce disease by insertional activation or mutation of cellular proto-oncogenes. These loci are identified as common viral integration sites in tumor DNAs. Here we report on the characterization of a novel common viral integration site in BXH-2 myeloid leukemias, designated Evi-2. Within the cluster of viral integration sites that define Evi-2, we identified a gene that has the potential for encoding a novel protein of 223 amino acids. This putative proto-oncogene possesses all of the structural features of a transmembrane protein. Within the transmembrane domain is a "leucine zipper," suggesting that Evi-2 is involved in either homopolymer or heteropolymer formation, which may play an important role in the normal functioning of Evi-2. Interestingly, the human homolog of Evi-2 has recently been shown to be tightly linked to the von Recklinghausen neurofibromatosis locus, suggesting a role for Evi-2 in human disease as well.

Original languageEnglish (US)
Pages (from-to)4658-4666
Number of pages9
JournalMolecular and Cellular Biology
Volume10
Issue number9
DOIs
StatePublished - Sep 1990

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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