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In mammalian cells, stress signaling usually leads to either cell-cycle arrest or apoptosis, depending on the severity of the insult and the ability of the cell to recover.
Indeed, double knockdown FLNabKD cells show somewhat reduced F-actin staining and in single FLNaKD cells stress fibres were thinner than those in wild-type cells (Baldassarre and Calderwood unpublished data).
In most cultured cells, stress fibres are linked to FA, where integrins cluster [ 15].
In a number of cells, stress fibres are completely de-polymerized showing only G-actin aggregates.
In cells, stress fiber networks are three-dimensional and are expected to exhibit considerably more complicated topologies.
Additional fumarate-induced cells stress in oligodendrocytes or neurons already exposed to severe oxidative injury might even increase demyelination or neurodegeneration.
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In cells, stress-induced electrolyte leakage is caused by the accumulation of ROS such as H2O2 and often results in decreased membrane permeability and programmed cell death (Neill et al. 2002; Demidchik et al. 2014).
However, unlike necrotic cells, stressed Scenedesmus cells maintained their cell membrane integrity until after 72 h of cultivation.
HUVEC cells stressed with 0,1% glutaraldehyde for 20 minutes on ice were used as positive control.
In nucleated cells, stress-activated p38 MAPK is involved in apoptosis, cytokine production, cytoskeleton reorganization, and transcriptional regulation.
In this study, we show that, in addition to reprogramming adjacent epithelial cells, stress-elicited factors from epithelial cells can also reprogram adjacent stromal cells.
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