In each marker result, the yield-positive allele of the genes was shown with a green letter.
After transfection of HEK-293 cells, one of the genes was shown to be active, yielding a 50% reduction of ALDH2 activity.
Expression of many MMPs-encoding genes was shown by microarray and qPCR analyses to increase in the migrating epithelium of wounded corneas.
The methylation profile of the analyzed genes was shown to be independent of age (Table 5).
The knockout of certain clock genes was shown to inhibit insulin secretion and trigger the onset of diabetes [9].
Knockdown of some of those actin-cytoskeleton-architecture-related genes was shown to increase oocyst numbers [16].
The regulation of both pilC1 and pilC2 genes was shown to be drastically different in the Nm2C4.3 strain [30] but was not investigated in the FAM20 strain.
Even so, mutation of either or both of these genes was shown to enhance biofilm formation in UAMS-1 albeit to a limited degree and only in the absence of plasma coating (Fig. 13).
Similarly the promoter region of the rDNA genes was shown to be located in the same region with a few conserved repeat sequences, which bind to Topoisomerase I [21].
Third, independently of our NESP55 data, other changes in gene expression support a chromaffin phenotype of hypoxic neuroblastoma cells: up-regulation of IGF2 and of HIF2α, in particular, was strong evidence of this, as chromaffin-specific expression within the sympathetic nervous system of both of these genes was shown both in this and in previous investigations [9], [44], [45].
In a previous report which evaluated expression of BMCC1-4 (BNIPXL) the BCH domain at the C-terminus, which is homologous to the BCH region of the BNIP2 and BPGAP1 genes, was shown to target Rho proteins with potential to inhibit cellular proliferation [24].
