Sentence examples for enhanced death from inspiring English sources

Downregulating PTK6 by either transfecting siRNA oligonucleotides or expressing an shRNA vector enhanced death of IGF-1R cells in suspension with enhanced detection of cleaved PARP product (Figure 2A and Figure S1C).

Shivpuri district further enhanced death notification by engaging NGOs to sensitize communities, including village nutrition and health workers and volunteers.

Enhanced death is also reported when ESFT cells are treated with TRAIL and bortezomib (Lu et al, 2008) or HDACi (Sonnemann et al, 2007).

Possible mechanisms of chemotherapy-induced enhancement of death receptor-induced apoptosis include p53-induced death receptor expression (e.g., Fas and TRAIL-R2) or enhanced death receptor signaling complex assembly and thus increased downstream caspase activation.

Withanolide E (the most active and abundant TRAIL-sensitizing withanolide isolated in this work) synergizes with TRAIL to induce cancer cell apoptosis in vitro and in vivo via enhanced death receptor-mediated TRAIL signaling.

Withanolide E, the most potent and least toxic of five TRAIL-sensitizing withanolides identified, enhanced death receptor-mediated apoptotic signaling by a rapid decline in the levels of cFLIP proteins.

Moreover, other HDAC inhibitors such as LAQ824, MS-275, FR901228, valproic acid and droxinostat have been shown to downregulate c-FLIP levels and enhance death receptor-induced apoptosis [46] [52].

RBC necroptosis induced by hCD59 signaling appears specific to damage by membrane pore formation, as CL-CD59 did not enhance death via eryptosis.

These observations are in agreement with other studies demonstrating that pretreatment of tumors with either bortezomib or depsipeptide enhances sensitivity to TRAIL-mediated killing, primarily by enhancing death receptors DR4 and DR5.

Breaking such resistance was rendered by some anticancer drugs that enhance death receptor expression and aggregation at the surface of tumor cells, thereby increasing the apoptotic response to death receptor ligands [ 8, 9].

Consistent with these data, simultaneous application of the inhibitory AhR antagonist α-NF to AhR-proficient HaCaT cells did also abolish the capacity of BP to enhance death receptor-induced apoptosis (Supplementary Figure 4).