Sentence examples for induction of sensitivity from inspiring English sources

As we previously demonstrated that the induction of sensitivity to tamoxifen by EBP1 was related to its effects on ErbB2 levels, we examined ErbB2 levels in both LTLT-Ca vector controls and EBP1 transfectants.

It is not clear whether these responses seen were due to induction of hormonal sensitivity through an unknown mechanism or due to regrowth of hormone-sensitive clones of cells which were previously suppressed by the original anti-androgen therapies.

The induction of TRAIL sensitivity by H. pylori is dependent on the activation of caspase-8 and its downstream pathway.

The results demonstrate that the overexpression of Bcl-2 in AGS cells inhibited the induction of TRAIL sensitivity in AGS cells by H. pylori.

This finding would suggest that EBP1-induced changes in expression of additional proteins may have a role in the induction of tamoxifen sensitivity by IPA.

The molecular downstream events that led to induction of tamoxifen sensitivity by the combination of IPA-3 and EBP1 overexpression are currently unknown.

However, in our previous study we demonstrated that induction of TRAIL sensitivity by H. pylori is independent of H. pylori virulent factors Vac A and Cag A. Therefore, the bacterial factors leading to induction of TRAIL sensitivity by H. pylori is still not clear, and it awaits further investigation.

Induction of drug sensitivity by an ALDH inhibitor, diethylaminobenzaldehyde (DEAB) resulted in significant reductions in cell viability but not a complete elimination of the sphere-forming cells, suggestive of the presence of a drug-resistant subpopulation.

As the ability of EBP1 to decrease ErbB2 levels has a role in its induction of tamoxifen sensitivity (Lu et al, 2011), we tested the effect of an EBP1 T261E phosphomimetic on ErbB2 levels.

The induction of TRAIL sensitivity by H. pylori is independent of the expression of H. pylori virulent factors Vac A and Cag A and is dependent on viable bacteria and direct contact with cells.

The phenomenon of induction of glucose sensitivity observed in glucose-resistant ß-cells is called glucose competence, i.e. the magnitude of the insulin secretion response to a rise in glucose concentration.