Research supported by MLC
The MLC supports the work of many research groups across a diverse range of disease areas, including hearing loss, type 2 diabetes, sex determination, neurodegeneration and circadian function, to name a few. Such support can include detailed phenotyping in addition to generation and husbandry of mutant mouse lines.
AKR1D1 knockout mice develop a sex dependent metabolic phenotype
Gathercole, L. L., Nikolaou, N., Harris, S. E., Arvaniti, A., Poolman, T. M., Hazlehurst, J. M., Kratschmar, D. V., Todorcevic, M., Moolla, A., Dempster, N., Pink, R. C., Saikali, M. F., Bentley, L., Penning, T. M., Ohlsson, C., Cummins, C. L., Poutanen, M., Odermatt, A., Cox, R. D., Tomlinson, J. W.
A Wars2 mutant mouse shows a sex and diet specific change in fat distribution, reduced food intake and depot-specific upregulation of WAT browning
Mušo, M., Bentley, L., Vizor, L., Yon, M., Burling, K., Barker, P., Zolkiewski, L. A. K., Cox, R. D., Dumbell, R.
Palmitoylated small GTPase ARL15 is translocated within Golgi network during adipogenesis
Wu, Y., Bai, Y., McEwan, D. G., Bentley, L., Aravani, D., Cox, R. D.
Maternal and offspring high-fat diet leads to platelet hyperactivation in male mice offspring
Gaspar, R. S., Unsworth, A. J., Al-Dibouni, A., Bye, A. P., Sage, T., Stewart, M., Wells, S., Cox, R. D., Gibbins, J. M., Sellayah, D., C, E. Hughes
Loss of O-GlcNAcase catalytic activity leads to defects in mouse embryogenesis
Muha, V., Authier, F., Szoke-Kovacs, Z., Johnson, S., Gallagher, J., McNeilly, A., McCrimmon, R. J., Teboul, L., van Aalten, D. M. F.