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.
Mouse Idh3a mutations cause retinal degeneration and reduced mitochondrial function
Findlay, A. S., Carter, R. N., Starbuck, B., McKie, L., Novakova, K., Budd, P. S., Keighren, M. A., Marsh, J. A., Cross, S. H., Simon, M. M., Potter, P. K., Morton, N. M., Jackson, I. J.
Mice with endogenous TDP-43 mutations exhibit gain of splicing function and characteristics of amyotrophic lateral sclerosis
Fratta, P., Sivakumar, P., Humphrey, J., Lo, K., Ricketts, T., Oliveira, H., Brito-Armas, J. M., Kalmar, B., Ule, A., Yu, Y., Birsa, N., Bodo, C., Collins, T., Conicella, A. E., Mejia Maza, A., Marrero-Gagliardi, A., Stewart, M., Mianne, J., Corrochano, S., Emmett, W., Codner, G., Groves, M., Fukumura, R., Gondo, Y., Lythgoe, M., Pauws, E., Peskett, E., Stanier, P., Teboul, L., Hallegger, M., Calvo, A., Chio, A., Isaacs, A. M., Fawzi, N. L., Wang, E., Housman, D. E., Baralle, F., Greensmith, L., Buratti, E., Plagnol, V., Fisher, E. M., Acevedo-Arozena, A.
Manipulation of dipeptidylpeptidase 10 in mouse and human in vivo and in vitro models indicates a protective role in asthma
Zhang, Y., Poobalasingam, T., Yates, L. L., Walker, S. A., Taylor, M. S., Chessum, L., Harrison, J., Tsaprouni, L., Adcock, I. M., Lloyd, C. M., Cookson, W. O., Moffatt, M. F., Dean, C. H.
Loss of p300 and CBP disrupts histone acetylation at the mouse Sry promoter and causes XY gonadal sex reversal
Carre, G. A., Siggers, P., Xipolita, M., Brindle, P., Lutz, B., Wells, S., Greenfield, A.
Leukemia Inhibitory Factor-Receptor is Dispensable for Prenatal Testis Development but is Required in Sertoli cells for Normal Spermatogenesis in Mice
Curley, M., Milne, L., Smith, S., Atanassova, N., Rebourcet, D., Darbey, A., Hadoke, P. W. F., Wells, S., Smith, L. B.