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The network impacts on cell cycle regulation and stops cell cycle progression if the DNA is damaged; this process is referred to as a DNA damage checkpoint.
Our findings indicate that Tan IIA inhibits cell proliferation, stops cell cycle progression, and induces apoptosis through the intrinsic mitochondrial pathway.
This CHX dose inhibits protein synthesis to ∼ 90% within 15 min [ 44] and stops cell cycle progression, as shown in histogram and density plots reported in Additional file 1. Cell cycle progression was monitored by measuring DNA content by FACS analysis, as previously described [ 45].
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A defective DDR makes cancer cells unable to effectively stop cell cycle progression, engage in DNA repair and/or trigger the apoptotic program when treated with DNA damaging drugs.
A common cellular response to radiation injuries is the activation of cell cycle checkpoints to stop cell cycle progression.
Loss of p21 results in decreased ability of the cell to stop cell cycle progression, possibly leading to carcinogenesis.
In that sense, telomeres might function as sensors of genotoxic stresses that permanently stop cell cycle progression should these stresses become too abundant.
An important part of the cellular response to DNA damage is to stop cell cycle progression when DNA damage is sensed.
In addition, the use of specific mTOR blockers stop cell cycle progression in the early G1 phase of the cell cycle, driving cells into G0 state promoting apoptotic processes [ 14, 15].
It is becoming increasingly evident, however, that telomeres not only count cell divisions, but also function as sensors of genotoxic stresses to stop cell cycle progression prematurely and long before cells would have entered replicative senescence.
Here, we review studies supporting the concept that telomeres are important cellular structures whose function not only is to count cell divisions, but also to act as molecular switches that can rapidly stop cell cycle progression permanently in response to a variety of stresses, including oncogenic signals.
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