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Your search keyword '"Bradley, Allan"' showing total 19 results
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19 results on '"Bradley, Allan"'

7. BRCTx Is a Novel, Highly Conserved RAD18-Interacting Protein

Author

Adams, David J., primary, van der Weyden, Louise, additional, Gergely, Fanni V., additional, Arends, Mark J., additional, Ng, Bee Ling, additional, Tannahill, David, additional, Kanaar, Roland, additional, Markus, Andrea, additional, Morris, Brian J., additional, and Bradley, Allan, additional

Published
2005
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10. Modeling del(17)(p11.2p11.2) and dup(17)(p11.2p11.2) Contiguous Gene Syndromes by Chromosome Engineering in Mice: Phenotypic Consequences of Gene Dosage Imbalance

Author

Walz, Katherina, primary, Caratini-Rivera, Sandra, additional, Bi, Weimin, additional, Fonseca, Patricia, additional, Mansouri, Dena L., additional, Lynch, Jennifer, additional, Vogel, Hannes, additional, Noebels, Jeffrey L., additional, Bradley, Allan, additional, and Lupski, James R., additional

Published
2003
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12. Mice Deficient for the Wild-Type p53-Induced Phosphatase Gene (Wip1) Exhibit Defects in Reproductive Organs, Immune Function, and Cell Cycle Control

Author

Choi, Jene, primary, Nannenga, Bonnie, additional, Demidov, Oleg N., additional, Bulavin, Dmitry V., additional, Cooney, Austin, additional, Brayton, Cory, additional, Zhang, Yongxin, additional, Mbawuike, Innocent N., additional, Bradley, Allan, additional, Appella, Ettore, additional, and Donehower, Lawrence A., additional

Published
2002
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18. Genetic Analysis of Mouse Embryonic Stem Cells Bearing Msh3and Msh2Single and Compound Mutations

Author

Abuin, Alejandro, Zhang, HeJu, and Bradley, Allan

Abstract

We have previously described the use of homologous recombination and CRE-loxP-mediated marker recycling to generate mouse embryonic stem (ES) cell lines homozygous for mutations at the Msh3, Msh2, and both Msh3andMsh2loci (2). In this study, we describe the analysis of these ES cells with respect to processes known to be affected by DNA mismatch repair. ES cells homozygous for the Msh2mutation displayed increased resistance to killing by the cytotoxic drug 6-thioguanine (6TG), indicating that the 6TG cytotoxic mechanism is mediated by Msh2. The mutation rate of the herpes simplex virus thymidine kinase 1 (HSV-tk1) gene was unchanged in Msh3-deficient ES cell lines but markedly elevated in Msh2-deficient and Msh3 Msh2double-mutant cells. Notably, the HSV-tk1mutation rate was 11-fold higher, on average, than that of the hypoxanthine-guanine phosphoribosyl transferase (Hprt) locus in Msh2-deficient cells. Sequence analysis of HSV-tk1mutants from these cells indicated the presence of a frameshift hotspot within the HSV-tk1coding region. Msh3-deficient cells displayed a modest (16-fold) elevation in the instability of a dinucleotide repeat, whereas Msh2-deficient andMsh2 Msh3double-mutant cells displayed markedly increased levels of repeat instability. Targeting frequencies of nonisogenic vectors were elevated in Msh2-deficient ES cell lines, confirming the role of Msh2 in blocking recombination between diverged sequences (homeologous recombination) in mammalian cells. These results are consistent with accumulating data from other laboratories and support the current model of DNA mismatch repair in mammalian cells.

Published
2000
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19. Inducible gene trapping with drug-selectable markers and Cre/loxP to identify developmentally regulated genes.

Author

Chen YT, Liu P, and Bradley A

Subjects
Animals, Base Sequence, Cell Differentiation drug effects, Cells, Cultured, DNA genetics, Female, Fetal Development genetics, Genes, Reporter drug effects, Genetic Markers, In Vitro Techniques, Integrases genetics, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Molecular Sequence Data, Phenotype, Pregnancy, RNA genetics, Retroviridae genetics, Tretinoin pharmacology, Gene Expression Regulation, Developmental drug effects, Genetic Techniques
Abstract

Gene trapping in mouse embryonic stem cells is an important genetic approach that allows simultaneous mutation of genes and generation of corresponding mutant mice. We designed a selection scheme with drug selection markers and Cre/loxP technology which allows screening of gene trap events that responded to a signaling molecule in a 96-well format. Nine hundred twenty gene trap clones were assayed, and 258 were classified as gene traps induced by in vitro differentiation. Sixty-five of the in vitro differentiation-inducible gene traps were also responsive to retinoic acid treatment. In vivo analysis revealed that 85% of the retinoic acid-inducible gene traps trapped developmentally regulated genes, consistent with the observation that genes induced by retinoic acid treatment are likely to be developmentally regulated. Our results demonstrate that the inducible gene trapping system described here can be used to enrich in vitro for traps in genes of interest. Furthermore, we demonstrate that the cre reporter is extremely sensitive and can be used to explore chromosomal regions that are not detectable with neo as a selection cassette.

Published
2004
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