We also saw numerous gene sets across both cell lines suggesting that HGF and VEGF signaling were differentially regulated under dcEFs, thus we have included an ATP-competitive inhibitor of both HGFR and VEGFR (mostly for MET, KDR, TIE2, and FLT4).
Separate mutations of the putative C/EBP binding site, c-myb-binding site or the GC-rich element resulted in a dramatically reduced transcriptional activity in both cell lines, suggesting cooperation between corresponding trans-factors.
While the extent of reconstitution efficacy varies between HeLa cells and HEK293 cells, the trend seen for N-, C- and untagged ATG16L1 is consistent between both cell lines, suggesting that the placement of epitope tags has adverse effects upon the autophagy efficacy of ATG16L1 constructs.
However, c-Myc expression was detected in both cell lines, suggesting that PIM kinase inhibition may be an effective therapeutic strategy in both VHL−/− and VHL+/+ tumours.
Double-immunofluorescence assays detected ΔNp63α and GLI2 in both cell lines suggesting the presence of a ΔNp63α-GLI2 signaxisg axin in OS cells.
In a general manner, the identification of numerous and diverse genes in both cell lines suggested that ECM mineralization is a complex process that requires tight regulatory mechanisms.
The proliferation response to graded amounts of these antibodies was identical in both cell lines suggesting that increased signaling alone is insufficient to cause the increased responsiveness (37).
However, activated Notch-2 was detected in both cell lines, suggesting that its activation, while possibly increased by SV40 ST, was not dependent on SV40 ST.
In contrast, Rapamycin slightly affected viral protein levels in both cell lines, suggesting that the increment of autophagy by EBV activation does not involve mTOR signaling.
