A
Allan Bradley
Researcher at Wellcome Trust Sanger Institute
Publications - 385
Citations - 81969
Allan Bradley is an academic researcher from Wellcome Trust Sanger Institute. The author has contributed to research in topics: Gene & Genome. The author has an hindex of 127, co-authored 379 publications receiving 77492 citations. Previous affiliations of Allan Bradley include Howard Hughes Medical Institute & University of Texas MD Anderson Cancer Center.
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Journal ArticleDOI
Molecular definition of multiple sites of antibody inhibition of malaria transmission-blocking vaccine antigen Pfs25.
S.W. Scally,Brandon McLeod,A. Bosch,Kazutoyo Miura,Qi Liang,Sean M. Carroll,Sini Reponen,Ngan Nguyen,Eldar Giladi,Sebastian Rämisch,Vidadi Yusibov,Allan Bradley,Franck Lemiale,William R. Schief,Daniel Emerling,Paul Kellam,C. Richter King,Jean-Philippe Julien +17 more
TL;DR: The crystal structure of Pfs25 is determined and antigenic sites that are recognized by transmission-blocking antibodies elicited in human immunoglobulin loci transgenic mice are identified and identified.
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α3-Integrins are required for hippocampal long-term potentiation and working memory
Chi-Shing Chan,Jonathan M. Levenson,Partha S. Mukhopadhyay,Lin Zong,Allan Bradley,J. David Sweatt,Ronald L. Davis +6 more
TL;DR: A postnatal forebrain and excitatory neuron-specific knockout of α3-integrin, one of several binding partners for β1 subunit is generated, suggesting that β1-integrins are the functional binding partner forβ1 for these processes in the forebrain.
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Null and conditional semaphorin 3B alleles using a flexible puroDeltatk loxP/FRT vector.
Louise van der Weyden,David J. Adams,Laura W Harris,David Tannahill,Mark J. Arends,Allan Bradley +5 more
TL;DR: A generic targeting vector, pFlexible, containing the positive/negative selectable marker puroΔtk and loxP and FRT recombination sites is developed and used to target Sema3B in ES cells, suggesting an inherent correction mechanism or level of redundancy between the class 3 semaphorins.
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Generation of a mouse model for citrullinemia by targeted disruption of the argininosuccinate synthetase gene.
TL;DR: This work has used homologous recombination in embryonic stem cells to generate a line of mice having a targeted disruption of the ASS gene and expects that these mice will serve as a useful model for exploring new treatments for citrullinemia including somatic gene therapy.
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Mouse chromosome engineering for modeling human disease.
TL;DR: The resulting mouse models are leading to a better understanding of the molecular and cellular basis of dosage alterations in human disease phenotypes, in turn opening new diagnostic and therapeutic opportunities.