scholarly journals MECOM (Ecotropic Viral Integration Site 1 (EVI1) and Myelodysplastic Syndrome 1 (MDS1-EVI1)

2017 ◽  
Author(s):  
Rotraud Wieser
Keyword(s):  
Myelodysplastic Syndrome ◽  
Integration Site ◽  
Viral Integration

scholarly journals Methodology and software to detect viral integration site hot-spots

2011 ◽  
Vol 12 (1) ◽  
Author(s):  
Angela P Presson ◽  
Namshin Kim ◽  
Yan Xiaofei ◽  
Irvin SY Chen ◽  
Sanggu Kim
Keyword(s):  
Hot Spots ◽  
Integration Site ◽  
Viral Integration

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

1990 ◽  
Vol 10 (9) ◽  
pp. 4658-4666
Author(s):  
A M Buchberg ◽  
H G Bedigian ◽  
N A Jenkins ◽  
N G Copeland
Keyword(s):  
Leucine Zipper ◽  
Transmembrane Domain ◽  
Integration Site ◽  
Transmembrane Protein ◽  
Structural Features ◽  
Viral Integration ◽  
Integration Sites ◽  
Leukemia Viruses ◽  
Common Integration Site

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.

scholarly journals The evolution of viral integration site analysis

Blood ◽  
2020 ◽  
Vol 135 (15) ◽  
pp. 1192-1193
Author(s):  
Stefan Radtke ◽  
Hans-Peter Kiem
Keyword(s):  
Integration Site ◽  
Viral Integration ◽  
Site Analysis ◽  
Integration Site Analysis

scholarly journals Ecotropic viral integration site 1, stem cell self-renewal and leukemogenesis

2012 ◽  
Vol 103 (8) ◽  
pp. 1371-1377 ◽  
Author(s):  
Keisuke Kataoka ◽  
Mineo Kurokawa
Keyword(s):  
Stem Cell ◽  
Integration Site ◽  
Viral Integration ◽  
Self Renewal

scholarly journals Spontaneous germ line virus infection and retroviral insertional mutagenesis in eighteen transgenic Srev lines of mice.

1989 ◽  
Vol 9 (1) ◽  
pp. 177-184 ◽  
Author(s):  
S E Spence ◽  
D J Gilbert ◽  
D A Swing ◽  
N G Copeland ◽  
N A Jenkins
Keyword(s):  
Dna Replication ◽  
High Frequency ◽  
Insertional Mutagenesis ◽  
Germ Line ◽  
Integration Site ◽  
Viral Integration ◽  
Mammalian Development ◽  
Copy Numbers ◽  
Cell Embryo ◽  
Dna Copy Numbers

SWR/J-RF/J hybrid mice spontaneously acquire new germ line ecotropic proviruses at high frequency. In the studies described here, we used these hybrids to produce 18 transgenic mouse lines, each carrying a single newly acquired Srev locus (SWR/J-RF/J ecotropic proviral locus). All of the newly acquired proviruses identified in mosaic founder SWR/J-RF/J mice that could be transmitted through the germ line were also present in somatic tissues, demonstrating that viral integration occurred before the germ line was set aside from the somatic lineages. Quantitative analysis of proviral DNA copy numbers in somatic and germinal tissues of mosaic founder parents combined with structural analysis of Srev loci indicated that these proviruses are acquired after multiple rounds of somatic viral reinfection and that most of these viral integration events occurred after DNA replication in the zygote and before DNA replication in the four-cell embryo. The frequency of provirus acquisition in Srev lines that expressed the infectious ecotropic virus was similar to that in SWR.RF mice carrying Emv-16 and Emv-17, suggesting that the chromosomal integration site of the parental locus is not an important determinant for high-frequency provirus acquisition. The frequency of recessive lethal mutations induced by spontaneous viral integration was 5%, which was similar to that induced by preimplantation embryo infection. This approach represents a simple and viable strategy for inducing and studying mutations that affect mammalian development.

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