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Thus, we hypothesized that adhesion-dependent regulation of PERK signaling might determine cell fate.
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Notably, differential CD95 ligation might also determine cell fate and apoptosis sensitivity outside the immune system.
We provide evidence for a dual role of p38 in cell cycle control and suggest that the level and/or the duration of p38 activation might determine the cell's decision to proliferate or to induce cell cycle arrest.
We hypothesized that the abundance of EndoG in normal conditions, which is regulated by CHIP, might determine whether cells readily undergo cell death in response to oxidative stress.
Also, the level of nuclear β-catenin and the origin of ES cells might determine how these cells respond to canonical Wnt signalling activation.
A possible explanation might be the altered expression of additional apoptosis-regulating factors that determine cell fate [ 30].
If the pathways that determine cell morphology also influence TN-C gene expression, we might expect a strong correlation between the two cellular parameters in each cell.
These factors which probably differ from tumour to tumour (or even from cell to cell) might determine whether the response to T-DM1 is apoptosis or MC.
HLA-DR/DQ alleles might determine CD4 T cells targeting of specific autoantigens and B* 39 alleles would then enhance CD8 T cells targeting of peptides of these autoantigens.
Thus, inherent properties of individual cell types, rather than specific cell death signals, might determine whether Akt is activated after cells are exposed to stresses.
These observations led to the hypothesis that the ratio of Mn to Fe in a cell might determine the relative abundance of different ROS induced during exposure to and recovery from IR [ 28, 29].
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