Admittedly, these experimental studies in mice will have limitations (32 ), but they should identify avenues for further research.
This comparison should identify any gene regulation in ob/ob mice that may be linked to the increased expansion of their β-cells.
Staff members should identify themselves.
A detailed roadmap of NPC disease neuropathology in mice should help to identify pathways conserved in humans that can mitigate disease and be successfully targeted by biopharmaceutical approaches.
It is probable that similar defects underlie LEOPARD syndrome in humans, so these mice should be useful for identifying and dissecting the signalling pathways affected by SHP-2 mutations.
The plasma proteins identified from these mice should correspond to a late stage subacute response to the carrageenan and associated sponge impact, rather than to initiation of the acute inflammatory response which occurs within 72 hours.
Future studies should address the functional consequences of these changes in lung structure in the DKO mice; they should also identify the cargo whose exocytosis is regulated by Rab27 and the molecular mechanisms by which this occurs.
Identifying the genetic modifiers that influence SCA1 phenotypes in mice should illuminate additional pathways that influence neurodegeneration.
Together, these efforts to genotype and phenotype mutant mice should provide additional data that could aid in validating candidate disease genes identified in GWAS.
