Faculty Research 1990 - 1999

Title

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

Document Type

Article

Publication Date

1990

Keywords

Animal, Base-Sequence, Cloning-Molecular, DNA-Probes, DNA-Viral: ge, Gene-Expression-Regulation-Viral, Gene-Library, Information-Systems, Leukemia-Experimental: ge, mi, Membrane-Proteins: ge, Mice, Mice-Inbred-Strains, Molecular-Sequence-Data, Mouse-Leukemia-Viruses: ge, Protein-Conformation, Proto-Oncogenes, Recombination-Genetic, Restriction-Mapping, Software, Support-U, S, -Gov't-P, H, S, Transcription-Genetic, Viral-Proteins: ge

JAX Location

1,972.

JAX Source

Mol Cell Biol 1990 Sep; 10(9):4658-66.

Grant

NO1-CO-74101, CA31101

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.

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