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The mechanisms of the ecotoxicological effects are well known and include oxidative and inflammatory processes, the release of genotoxic compounds [16], inducing mitochondrial dysfunction [18], destabilization of cell membranes, denaturation of proteins, and even the deterioration of DNA [16, 32].
The mechanism of ECP-triggered cell damage is suggested to involve destabilization of cell membrane lipids through pore formation, causing changes in membrane permeability and membrane leakage [ 5, 12, 20].
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Previously, PAK1 was shown to contribute in the destabilization of cell-to-cell contacts in keratinocytes [33].
Furthermore, since CA-4-P interferes with the formation of stress fibers, it inhibits the VE-cadherin/ β-catenin complex, thus leading to the destabilization of cell-cell junctions and increasing endothelial permeability [ 54].
On the other hand, a study has reported that in LNCaP prostate cancer cells and MDA-MB-231 breast cancer cells, the ligand-mediated activation of EPHA2 promotes the nuclear translocation and phosphorylation of ERK kinases, followed by the increased nuclear translocation of the Elk-1 transcription factor and the consequent destabilization of cell-ECM attachment [81].
Activation of SFKs is associated with increased tumor invasion and metastasis through initial destabilization of epithelial cell-cell junctions.
Hence, a decrease in the levels of these polycations might cause a destabilization of important cell structures, leading to alterations in cell integrity and inducing cell death.
While VEGF-A and Ang-2 are involved in the destabilization of endothelial cell junctions, sFlt-1 and Ang-1 present distinct functions, stabilizing the endothelial barrier.
The possibility that a deficiency in IL-6 may destabilize tTreg-cell function in vivo was further tested by de novo induction of Treg cells in vivo and in vitro; as these processes occurred normally in mice deficient in IL-6, destabilization of Treg-cell function must occur within the tTreg-cell population, as postulated elsewhere [ 42].
Transfer of stem cell populations into environments that promote differentiation leads to destabilization of stem cell-like states.
MDSCs are classically known to decrease CTL response, mostly through destabilization of T-cell receptors and decreased expression of certain CD3 subtypes, ultimately leading to CTL apoptosis.
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