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It is important to distinguish this new role of CN during the early UPR from its distinct cell death function during later time points of the UPR.
We have convincingly demonstrated that NF-κB has a pro-cell death function in response to chronic insult with H2O2 in MEFs.
Furthermore, Notch signaling is well known to play an important role in anti-cell death function under mechanical stress [26], [28], which consistent with our results.
Previous reports of NF-κB's pro-cell death function have been shown to depend on either basal [24], [25] or activated NF-κB [49].
Due to technical difficulties reconstituting p50 into nfkb−/− cells, we were unable to distinguish whether NF-κB's pro-cell death function is due to RelA homodimer or the p50 RelA heterodimer.
Although there have been a few reports addressing the pro-cell death role of NF-κB, the precise mechanism of NF-κB's pro-cell death function still remains elusive.
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In this context mitochondria are known as regulators of cell death functioning as a node where signals are integrated.
In the hospital room, grief conspired with natural curiosity: so this is how a body near death functions; this is how most of us will go. . . .
In the hospital room, grief conspired with natural curiosity: so this is how a body near death functions; this is how most of us will go...
Death (red) is determined by loss of fluorescent intensity (neuron 7, day 3) or changes in morphology (neuron 15, day 6), and time of death for each cell is used to estimate the cumulative (b,e) and instantaneous (d,g) risk of death functions.
(PDF 187 KB) 40635_2014_20_MOESM4_ESM.pdf Additional file 4: Table S3.: Significant 'cell death' functions in septic shock patients over time compared to healthy volunteers.
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