Non-homologous end joining mediated DNA repair is impaired in the NUP98-HOXD13 mouse model for myelodysplastic syndrome
Copyright policy )Non-homologous end joining mediated DNA repair is impaired in the NUP98-HOXD13 mouse model for myelodysplastic syndrome
Chromosomal translocations typically impair cell differentiation and often require secondary mutations for malignant transformation. However, the role of a primary translocation in the development of collaborating mutations is debatable. To delineate the role of leukemic translocation NUP98-HOXD13 (NHD13) in secondary mutagenesis, DNA break and repair mechanisms in stimulated mouse B lymphocytes expressing NHD13 were analyzed. Our results showed significantly reduced expression of non-homologous end joining (NHEJ)-mediated DNA repair genes, DNA Pkcs, DNA ligase4, and Xrcc4 leading to cell cycle arrest at G2/M phase. Our results showed that expression of NHD13 fusion gene resulted in impaired NHEJ-mediated DNA break repair.
- Virginia Tech United States
- Wake Forest University United States
- Edward Via College of Osteopathic Medicine United States
- Molecular Pathology Laboratory Network (United States) United States
Homeodomain Proteins, DNA End-Joining Repair, Cell Cycle Checkpoints, Translocation, Genetic, Nuclear Pore Complex Proteins, Mice, Myelodysplastic Syndromes, Animals, DNA Breaks, Double-Stranded, Gene Fusion, Transcription Factors
Homeodomain Proteins, DNA End-Joining Repair, Cell Cycle Checkpoints, Translocation, Genetic, Nuclear Pore Complex Proteins, Mice, Myelodysplastic Syndromes, Animals, DNA Breaks, Double-Stranded, Gene Fusion, Transcription Factors
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