Using Fucci reporter mice that enable in vivo visualization of cell-cycle status, we detect increased proliferation during pre-HSC expansion followed by a slowing down of cycling once cells start to acquire a definitive HSC state, similar to fetal liver HSCs.
To overcome these problems, the investigators generated conditional Brca1 knockout mice that enable tissue-specific inactivation of BRCA1 by Cre recombinase-mediated deletion of one or more Brca1 exons flanked by loxP recombination sites (Jonkers and Berns, 2002).
By identifying key tissues through serial microPET imaging, ROIs were established in each mouse that enabled the quantification of tissue concentration as a function of time.
Here we generated an E-cadherin-GFP mouse that enables intravital photobleaching and quantification of E-cadherin mobility in live tissue without affecting normal biology.
A new transgenic mouse that enables tissue-specific GFP labeling of cilia creates new opportunities for using live imaging to understand cilium function and to better characterize the many genetic models of ciliopathies.
We used a transgenic mouse system that enabled isolation of small numbers of Oct4ΔPE GFP-positive germ cells in vivOct4ΔPE GFP-positiveferentiation from mESCs in vitro, to uncover quantitate and qualitative phenotypes associated with the disruption of a singermtranslational regulator, Dazl.
We have therefore now performed an experiment similar to that of Malanchi et al (2008), using a genetically modified mouse line that enabled us to study the effect of a tamoxifen-induced, hepatocyte-specific knockout of Ctnnb1 during chemical hepatocarcinogenesis.
To assess whether insertion of an ID element has the potential to impart dendritic localization, we generated transgenic mice with constructs that enabled us to test a somatic mRNA for potential acquisition of dendritic transport competence by inserting ID elements or the entire coding region of BC1 RNA into the 3' UTR of the reporter mRNA.
To understand how the complex network of DC lineages is generated in a model system, we engineered an Id2-GFP mouse reporter strain that enabled us to track endogenous Id2 expression on a single cell level during DC differentiation.
Since endothelial-specific deletion of FAK induces lethality during mouse embryonic development (Braren et al, 2006; Cohen & Guan, 2005; Ilic et al, 1995), we have generated a new mouse model that enables us to induce endothelial FAK deletion in adult mice upon tamoxifen treatment.
