Abnormality in DNA-protein binding in ataxia-telangiectasia nuclear extracts.
Anomalies in DNA replication, repair and recombination in ataxia-telangiectasia (A-T) point to a defect in structure or function of chromatin. In this study we have compared DNA-protein binding in nuclear extracts from control and A-T cells using two assay systems, filter-binding and DNA-accessibility. Interestingly, the extent of DNA protein binding over a range of protein concentration was significantly lower in A-T extracts. In addition the accessibility of the restriction enzyme Eco R1 to protein-bound plasmid was greater when A-T extracts were used. This is in keeping with the reduced binding observed in the filter-binding assay.
Mohamed
R
R
Department of Biochemistry, Faculty of Life Sciences, Universiti Kebangsaan, Malaysia.
Lavin
M F
MF
D001260:Ataxia Telangiectasia / Q000378:metabolism*; D002460:Cell Line; D002461:Cell Line, Transformed; D002467:Cell Nucleus / Q000378:metabolism*; D004247:DNA / Q000378:metabolism*; D004268:DNA-Binding Proteins / Q000378:metabolism*; D015246:Deoxyribonuclease EcoRI / Q000378:metabolism; D004854:Herpesvirus 4, Human; D006801:Humans; D010957:Plasmids; D011485:Protein Binding
D004268:DNA-Binding Proteins; D004247:DNA; D015246:Deoxyribonuclease EcoRI