Given our findings that the expression of vtrB is under control of VtrA (Fig. 3) and that vector-expressed vtrB could restore the defect in enterotoxicity of the WTΔvtrAΔvtrB strain (Fig. 5B), VtrB might determine this specific gene expression.
Thus, we expressed M3-APC in HCT116βw cells (HCT116 cells that contain only a wild-type allele of β-catenin) to determine whether this expression altered cell cycle progression.
We then used the antibodies to determine if this expression was consistent in a series of adult brains.
To determine if this expression pattern is conserved across species, we examined the expression of human HKGs orthologs in mouse, rat, and dog gene expression profiling data sets (unpublished data) for these species (Table 2).
In this study, we aimed to determine the expression of this transcriptional factor in colorectal tumours.
Having established that, in murine islets, GPR120 is primarily expressed in delta cells and that it may regulate somatostatin secretion, it was considered important to extend this analysis to determine the expression patterns of GPR120 in human islet cells.
In the study presented here, we sought to determine this potential relationship between fascin expression and malignant progression in colorectal adenomas.
Then, we prove that the same method can be extended for the exponential window case, while the main difference here is that we are able to use the implicit expressions to determine this Borel set.
The energy gap (Eg) could be determined from this expression by using the values of ε1 0) and the plasma energy hωp.
It remains to be determined if this expression is localized to the premigratory neural crest in the dorsal part of human neural tube.
