While studying the genetic basis for VPA teratogenicity in mice, we discovered that parental factors influence fetal susceptibility to induced malformations.
While investigating the thymic phenotype of Id3−/− mice we discovered that the number of γδ T cells is increased by approximately 8 fold (range 3- to 15-fold) compared to Id3+/+ mice (Fig. 1A and B).
When analyzing the 4 month old Cln1-/ mice we discovered upregulation of inflammation associated pathways.
Having confirmed that BCG induces a sickness response in C57BL/6 and WT mice as much as it does in CD1 mice, we discovered that NPY and PYY play a role in regulating the biological responses to BCG.
In our current study with attenuated TGFβ signaling in MMTV-c-Neu mice, we discovered an opposite effect in which levels of CXCL1/CXCL5 as well as CCL2 (MCP-1) decreased in parallel with an increased level of VEGF.
Through systematically phenotyping organ systems in Sun1 −/− mice, we discovered that the average weight of the brains of adult Sun1 −/− (n=12, 402.0±7.2 mg) mice was significantly lower than wild-type (WT) counterparts (WT, n=10, 449.2±5.1 mg, P<0.001; supplementary material Fig. S1A,B).
By studying mammary development in MMTVrtTA/H2BGFP transgenic mice, we discovered a subset of CD24+/CD29lo cells possessing the unique ability to develop small, multilineage mammary outgrowths, ranging in size from a small alveolar cluster to a half-grown mammary gland, that can produce milk, yet have no self-renewal activity.
Using a Nf1 heterozygous mouse model, we discovered a striking phenotype whereby OPCs formed discrete, hyperdense foci.
Of special note, nine of the unannotated mouse models we discovered (discussed earlier) encode predicted proteins with fingerprint patterns that match annotated genes in human and other species extremely well.
