Non-homologous end joining mediated DNA repair is impaired in the NUP98-HOXD13 mouse model for myelodysplastic syndrome

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• 作者：Abdul Gafoor Puthiyaveetil^a ; ^b ; Christopher M. Reilly^c ; Timothy S. Pardee^d ; David L. Caudell^a ; ^b ; ^{dcaudell@vt.edu}
• 关键词：Chromosomal translocation ; NUP98 ; HOXD13 ; DNA double strand break ; Non-homologous end joining
• 刊名：Leukemia Research
• 出版年：2013
• 出版时间：January, 2013
• 年：2013
• 卷：37
• 期：1
• 页码：112-116
• 全文大小：533 K

文摘

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.