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Many studies provide tantalizing evidence that small-molecule drugs can restore the activity of p53 and activate apoptosis in mutp53-carrying tumor cells.
Most cytotoxic drugs, which activate apoptosis, lead to the activation of the mitochondrial pathway.
There are a plethora of routes by which anticancer agents or radiotherapy can activate apoptosis, normally characterized by activation of intrinsic or extrinsic pathways.
In fact, the autophagy that is induced by DT-EGF in U87MG cells inhibits caspase activation and thus explains why they don't activate apoptosis.
Individual cells activate apoptosis in a step-like manner; however the time of activation differs.
The QDs increase the intracellular ROS level and activate apoptosis.
To activate apoptosis in tumors, SMAC mimetic compounds (SMCs) have disappointing effects as single agents in tumors with low expression of death-inducing proteins.
Apoptotic staining, DNA fragmentation, and flow cytometry analysis further demonstrate that treatment of Cdte QDs together with DNR can clearly activate apoptosis in HepG2/ADM cells.
This may indicate that NP-Pt analogs to platinum-based drugs, where Pt exists in cationic form, activate apoptosis and at the same time suppress proliferation.
One fundamental reason for treatment failure is that it is designed to activate apoptosis genes (eg, TP53) that may be unavailable because of mutation or deletion.
In these stages the sFasL generated by MMP7 could activate apoptosis, allowing the survival of cells that do not activate apoptosis via Fas [4].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com