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Identification of candidate target genes for EVI-1, a zinc finger oncoprotein, using a novel selection strategy

J H Kim1, P Hui, D Yue

  • 1Yale University, Department of Pathology, New Haven, Connecticut 06520-8023, USA.

Oncogene
|October 30, 1998
PubMed

Insights

Researchers identified EVI-1 (Ecotropic Viral Integration 1) target genes in mice, estimating ~4300 binding sites. They isolated novel genes, including Itpr2, crucial for myelopoiesis, and demonstrated EVI-1

Area of Science:

  • Molecular Biology
  • Genomics
  • Cancer Research

Background:

  • The zinc finger protein Ecotropic Viral Integration 1 (EVI-1) is implicated in myelogenous leukemia development in both mice and humans.
  • Identifying EVI-1 target genes is crucial for understanding its role in leukemogenesis.

Purpose of the Study:

  • To identify and isolate target genes regulated by the EVI-1 protein.
  • To estimate the number of EVI-1 binding sites in the mouse genome.

Main Methods:

  • A two-step selection process was employed: genomic fragment selection for high-affinity EVI-1 binding, followed by cDNA hybrid selection.
  • Construction of a sublibrary of genomic fragments enriched for EVI-1 binding sites.
  • Utilizing a tetracycline-regulated system to control a chimeric EVI-1-VP16-fusion protein for gene regulation studies.

Main Results:

  • An estimated 4300 EVI-1 binding sites per haploid mouse genome were identified.
  • A sublibrary of genomic fragments containing a significant fraction of EVI-1 binding sites was constructed.
  • Novel genes, including Itpr2 (inositol trisphosphate type two receptor), were isolated and found to be transcriptionally regulated during myelopoiesis.
  • The chimeric EVI-1-VP16 activator directly regulated Itpr2 expression.

Conclusions:

  • The study successfully identified target genes for the EVI-1 protein using a novel genomic selection strategy.
  • Itpr2 is a novel EVI-1 target gene transcriptionally regulated during myelopoiesis.
  • These findings provide insights into the molecular mechanisms of EVI-1 in leukemogenesis and offer potential targets for therapeutic intervention.

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