Using the MMTV-PyMT model of metastatic breast cancer in mice, we have shown that (R -[11C]PAQ can visualize lesions with aR -[11C]PAQoing neovascanarization.
In these mice we have now the opportunity to follow PDAC evolution in the living animal in a time frame process.
Taking advantage of homogeneously marked cells from green fluorescent protein (GFP) transgenic mice, we have previously demonstrated that bone marrow-derived stromal cells (BSCs) differentiate into a variety of cell lineages both in vitro and in vivo.
Taking advantage of homogeneously marked cells from green fluorescent protein (GFP) transgenic mice, we have recently reported that adipose-derived stromal cells (ASCs) could differentiate into mesenchymal lineages in vitro.
Using genetic engineering in mice, we have generated and characterized approximately 20 Cre and inducible CreER knockin driver lines that reliably target major classes and lineages of GABAergic neurons.
The conditonal Fto knockout mice we have generated will be helpful in that regard.
Using tissues from multiple lines of knockout mice we have examined genome-wide changes in gene expression.
In these aged mice we have previously reported the occurrence of abnormal tau hyperphosphorylation at different sites [17].
Using a large data set of CNVs discovered in strains of inbred mice, we have quantified factors that contribute to discrepancies between aCGH studies.
In the spinal cord of G93A SOD1 mice we have observed progressive accumulation of Triton-insoluble proteins: mutant SOD1, its oligoubiquitinated forms and other unknown proteins [5], [15].
In the previous paper demonstrating the phenotype of K14-Cdk2ap1 mice, we have observed the overexpression of Cdk2ap1 in epithelial tissues [12].
