Disease relevance of Evi2a

• Approximately 15% of BXH-2 myeloid leukemias harbor proviral integrations at the Evi-2 common viral integration site [1].
• We present a model that accounts for the positive selection of MRV proviruses at Evi-2, which may allow selective identification of common viral integration sites harboring tumor suppressor genes [2].
• Evi-2, a common site of viral integration in BXH-2 myeloid lymphomas, is located within a large intron of the Nf1 tumor suppressor gene [2].

High impact information on Evi2a

• Viral integration at Evi-2 appears to induce disease by disrupting normal Nf1 expression [2].
• D11Nds1 and Evi-2/D11Mit34 thus define the new proximal and distal boundaries, respectively, for the nu interval [3].
• Mice that carried recombinational breakpoints between D11Nds1 and D11Mit8 were further analyzed at the loci Evi-2 and D11Mit34, which placed nu 0.2 cM proximal to these markers [3].
• Mapping of the gene for inducible nitric oxide (NO) synthase of mouse macrophages to chromosome 11, close to Evi-2, nu, and Idd-4 [4].
• As part of our exploration of this region, we have mapped the human homolog of a murine gene (Evi-2) implicated in myeloid tumors to a location between the two translocation breakpoints on chromosome 17 [5].

Biological context of Evi2a

• As part of experiments to determine whether Evi-2 identified a new proto-oncogene locus involved in myeloid disease, we determined its chromosomal location [6].

Anatomical context of Evi2a

• Retroviral integration at the Evi-2 locus in BXH-2 myeloid leukemia cell lines disrupts Nf1 expression without changes in steady-state Ras-GTP levels [1].

Other interactions of Evi2a

• A common site of ecotropic murine leukemia virus integration designated Evi-2 (ecotropic viral integration site-2) has been identified in BXH-2 myeloid tumors [6].

References