Genomic instability in Gadd45a-deficient mice
Autor: | Chu-Xia Deng, Sheikh Ms, K. Lundgren, Qimin Zhan, Pedro M. Fernández-Salguero, E. Tolosa, W. F. Morgan, Jonathan D. Ashwell, T. A. Molinaro, L. Augeri-Henmueller, Dmitry V. Bulavin, Albert J. Fornace, R. Shehee, M. P. Rosenberg, K. E. Kim, M C Hollander |
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Rok vydání: | 1999 |
Předmět: |
Male
Genome instability Aneuploidy Apoptosis Biology Spindle pole body Mice Neoplasms Chromosome instability Gene duplication Genetics medicine Animals Mitosis Cellular Senescence Centrosome Mice Knockout Cell Cycle G1 Phase Intracellular Signaling Peptides and Proteins Proteins Fibroblasts Embryo Mammalian medicine.disease Mice Inbred C57BL Cell Transformation Neoplastic Genes ras Phenotype Gamma Rays Female Thymus Hyperplasia Cell Division Gene Deletion Cytokinesis |
Zdroj: | Nature Genetics. 23:176-184 |
ISSN: | 1546-1718 1061-4036 |
DOI: | 10.1038/13802 |
Popis: | Gadd45a-null mice generated by gene targeting exhibited several of the phenotypes characteristic of p53-deficient mice, including genomic instability, increased radiation carcinogenesis and a low frequency of exencephaly. Genomic instability was exemplified by aneuploidy, chromosome aberrations, gene amplification and centrosome amplification, and was accompanied by abnormalities in mitosis, cytokinesis and growth control. Unequal segregation of chromosomes due to multiple spindle poles during mitosis occurred in several Gadd45a -/- cell lineages and may contribute to the aneuploidy. Our results indicate that Gadd45a is one component of the p53 pathway that contributes to the maintenance of genomic stability. |
Databáze: | OpenAIRE |
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