Dr, Transgenic Core Head
Genetically modified models represent one of the most powerful methods of functional gene analysis in vivo. Furthermore, the ability to introduce specific mutations into the genome enables models of human disease to be generated, facilitating insights into the pathophysiology of disease and providing a model with which therapeutic strategies and diagnostic tools can be optimized.
Our group provides groups within Oxford University access to transgenic technologies both on a fee-for-service type arrangement and on a collaborative basis. Technologies offered include embryo microinjection, embryonic stem cell transfection, Knock-out/-in construct design and in vivo shRNA mediated gene Knock-down. In addition, embryo rederivation and cryoconservation services are offered to facilitate the management, transfer and security of genetically modified strains.
The research activity of the group is focused on the development of novel methodologies for the generation of genetically modified models. The aims being to improve the reliability of the technology and to reduce the animal cost of research involving genetically modified models.
|Fluorescent 1 and 2 cell embryos|
|A single ES cell colony expressing Green Fluorescent Protein growing on a fibroblast feeder layer|
|Microinjection of embryonic stem cells into a blastocyst|
Electroporation and genetic supply of Cas9 increase the generation efficiency of CRISPR/Cas9 knock-in alleles in C57BL/6J mouse zygotes.
Alghadban S. et al, (2020), Scientific reports, 10
Regulation of substrate choice contributes to the regulation of glucagon secretion from alpha cells in response to glucose
Armour SL. et al, (2020), DIABETOLOGIA, 63, S70 - S71
The Configuration of RPA, RAD51, and DMC1 Binding in Meiosis Reveals the Nature of Critical Recombination Intermediates
Hinch AG. et al, (2020), Molecular Cell, 79, 689 - 701.e10
RNAseq reveals mechanisms of cardiomyopathy in Mlp-C58G knock-in mice
Ehsan M. et al, (2020), JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 140, 53 - 53
Phenotype of a transient neonatal diabetes point mutation (SUR1-R1183W) in mice
Sachse G. et al, (2020), Wellcome Open Research, 5, 15 - 15