Elevated progesterone levels during pregnancy have been shown to sensitize the maternal myocardium to cocaine-induced catecholaminergic effects; the greater sensitivity of fetal heart ODC to cocaine, as compared to neonatal heart, supports the hypothesis that similar enhancement of fetal cardiac irritability can contribute to cocaine-induced cell damage.
Loss of cFLIP alone has been shown to sensitize ACHN cells to TRAIL16.
Inhibitors of PI3K, Akt and mTOR have been shown to sensitize selected tumor cells to cytotoxic drugs through multiple downstream effects.
Since other protein synthesis inhibitors have been shown to sensitize various cells (including ACHNs) to TRAIL-induced apoptosis via down-regulation of cFLIP, a quantitative western blot assay was used to determine the effects of the rocaglates on protein expression of cFLIP.
The cytokine release from SGC has been shown to sensitize nociceptive neurons in the TG [12].
Elevated CHOP levels have also been shown to sensitize cells to oxidative insults (Ikeyama et al., 2003) and increase ROS levels in rat fibroblasts (McCullough et al., 2001).
NF-κB inhibition has been shown to sensitize SKBr3 cells to TNFα [48], [49].
ANG-2 has also been shown to sensitize endothelium to the effects of TNF [50].
Recently, the peptide amylin has been shown to sensitize animals and humans to the effects of leptin[43], [44].
Furthermore, Lapatinib has been shown to sensitize cancer cells to chemotherapeutic drugs by inhibiting the EGFR, P-glycoprotein (Pgp) and breast cancer resistance protein (BCRP) [24].
Second, Chk1 inhibition by UCN-01 or other chemical Chk1 inhibitors has been shown to sensitize preferentially p53-deficient cells [38] [40].
