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Recent studies using the Aire knockout mouse have demonstrated gene-dose dependency and disease modifier loci, returning the onus of exploration to human genetics.
Johnson and Tilly have argued that their experiments in the adult female mouse have demonstrated conclusively that neo-oogenesis continues in adulthood.
Investigations in a Crx-knockout mouse have demonstrated a central role of Crx in the developing rodent visual system.
Gene knockout studies in laboratory models such as zebra fish and mouse have demonstrated that miRNAs are involved in development through post-transcriptional regulation of mRNA expression [ 17, 18].
Studies in model organisms including Xenopus and mouse have demonstrated key roles for Sonic Hedgehog itself, and for Foxf1, in mediating mesoderm endoderm cross talk during very early development of the gut tube.
To date, many different endothelial cell types, including both human and mouse, have demonstrated EndMT when exposed to TGF- β or Notch ligands in vitro (Frid et al, 2002; Ishisaki et al, 2003; Noseda et al, 2004; Timmerman et al, 2004; Zeisberg et al, 2007a, 2007b).
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The Aire knockout mouse has demonstrated that Aire initiates immune tolerance via promiscuous transcription of organ-specific genes in the thymus.
Retrospective clonal analysis in the mouse has demonstrated that the posterior spinal cord neurectoderm and paraxial mesoderm share a common bipotent progenitor.
While this manuscript was under review, a study in the mouse has demonstrated that Cx43 in gut endoderm is required for information relay from the PNC / node to the LPM (Viotti et al., 2012), demonstrating evolutionary conservation of mechanisms.
Similarly, but with a different twist, AAV-delivered antibodies to the nasal passages of mice have demonstrated excellent prophylaxis against flu virus (Limberis et al., 2013; Balazs et al., 2014; Adam et al., 2014).
Notably, [18F]FLT PET scans in NSCLC tumor-bearing mice have demonstrated their utility in identifying TKI-resistant tumors, which harbor the most frequently encountered mutations associated with TKI resistance, i.e., the secondary T790M mutation [44] and MET amplification [43].
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