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To demonstrate that induction of caspase 2 and 3 activities were specific, we treated MON cells in the presence and absence of p53 and also in the presence and absence of specific caspase 2 or 3 inhibitors.
The results of the study demonstrate that induction of OHC apoptosis after the noise exposure is an extremely rapid process.
We demonstrate that induction of a specific subset of cytokines is dependent upon integrin α3β1-mediated endocytosis of the ligand.
Investigations were conducted in a similar manner using two other donors, SNOG and SNAP to demonstrate that induction of apoptosis markers could occur with other NO donors.
These results demonstrate that induction of autophagy prior to intoxication protects cells from vacuolation but does not inhibit the post-mitotic vacuolation.
We further demonstrate that induction of p27Kip1 expression by Stat1 is essential for the suppression of Ras-mediated oncogenesis in vitro and in vivo via mechanisms that are affected by the phosphorylation of Stat1 at tyrosine 701 and serine 727.
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We were, however, not capable of demonstrating that induction of more apoptosis or more necrosis results in differences in transepithelial passage of antibiotics.
These results demonstrated that induction of IL-6 occurred somewhere between 100 fg/mL and 1 pg/mL.
Data was generated that demonstrated that induction of mitochondrial swelling along with enhanced Hsp70 and 90 expression could be reproduced in another rat glioma cell line, F98.
Our previous study demonstrates that induction of NKG2D ligands in the WSX1-engineered TC1 and AT84 tumor cells are associated with tumor growth inhibition [12].
Our earlier studies demonstrated that induction of I/R in the intact murine heart resulted in significant upregulation of RAGE, particularly in cardiomyocytes.
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