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In contrast, 1,25D failed to increase the expression of differentiation markers in blast cells isolated from patients carrying activating mutations in Flt3 gene.
However, hyperglycemia failed to increase the expression of cTnI when GATA-4 was silenced by small interfering RNA (siRNA) in H9c2 cells.
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In cells treated with chronic morphine, the expression of CREB, adenylyl cyclase (AC) and protein kinase A (PKA) were increased, while in cells infected with LV-CREB3, treated with chronic morphine treatment failed to increase the expressions of CREB and AC.
However, ATF4 overexpression failed to increase the expression level of a series of proangiogenic factors including vascular endothelial growth factor A (VEGFA) in tumor cells in this model.
When testing the effectiveness of the three siRNAs towards reducing the expression level of Bmi1 protein, we found that X164, the only siRNA that failed to increase the efficacy of VM26, also failed to reduce expression of Bmi1 protein (Fig. 2A lower panel).
Importantly, we found that exogenous expression of FE-BRCA2 variants with the BRC mutations and/or the TR2 mutation failed to increase the level of pS14-Rad51.
These data suggested that the GATA3/R299Q protein failed to increase the PTH gene expression.
Co-expression of HLA-DR and TLR7 failed to increase the TNF response compared to TLR7 positive cells.
GFT505 failed to increase significantly the expression of PPARα and PPARδ target genes, such as CPT1a, CPT1b, PDK4, and CD36.
Addition of aggregated Aβ to primary microglia and BV-2 cells failed to increase expression of TREM2 or Tmem176b (data not shown).
Figure 3 shows that CM from WT Bowes cells (clone 8) failed to increase expression of CXCR4, and its ligand SDF-1.
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