for formal expression of specifications within a regression framework.
Expression of EC specification and marker genes was monitored by quantitative PCR, western, immunocytochemistry, and flow cytometry.
Previous studies have shown that REST represses the expression of neuronal specification genes in mouse ES cells, while differentiation of ES cells into neurons results in proteasomal degradation of REST and subsequent transcriptional activation of several target genes [49].
Our data supports the hypothesis that differential developmental gene expression may drive invasive potential in metastatic melanoma, and that melanoma heterogeneity may be explained by the differing capacity of melanoma cells to both withstand decreased expression of lineage specification genes and to respond to the tumour microenvironment.
Expression of neural specification genes (Table 5 and 7) and neurotrophic/growth factor genes (Table 4 and 7) was also reduced by the ethanol exposure.
Within 24 hours, Lhx1 overexpression sustained expression of NR specification genes in addition to Chx10, such as Rx1, Six3, Six6, and Sox2.
The ability to induce NR formation was mediated by expression of NR specification genes (Rx1, Six3, Six6, Chx10, Sox2) at least in early stages but also likely mediated by induction of unidentified secreted factors.
We next examined whether ectopic NR formation after Lhx1 overexpression was mediated by expression of NR specification genes such as Rx1, Six3, Six6, Chx10 and Sox2 (Ishii et al., 2009; for a review, see Locker et al., 2009).
To investigate whether the expression of skeletogenesis specification genes was also delayed, we searched for an early skeletogenesis marker osterix (osx), a marker of the intermediate stages of skeletogenesis collagen 1 (colI), and also a late differentiation marker involved in mineralisation, osteonectin (osn) at 24 and 48 hpc by in situ hybridization (Fig. 4A L).
To mitigate these problems, we divided the expression of a protocol specification into two parts.
