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ATM (Ataxia Telangiectasia Mutated) is an essential checkpoint kinase that signals DNA double-strand breaks in eukaryotes.
For the essential checkpoint proteins, Mad2 and Cdc20, we present the mutation effect on our model in detail in Figure 4 for the Convey variant.
Subsequently, cells were forced to exit mitosis by addition of SP600125, which inactivates the spindle assembly checkpoint by direct inhibition of the essential checkpoint kinase Mps1 [46].
To keep the IFN activation in balance, there are a set of different cellular deubiquitinases, such as A20, CYLD, YopJ and deubiquitinating enzyme A (DUBA), that maintain the activation homeostasis of each essential checkpoint factors aforementioned [17], [20] [23].
The Ataxia Telangiectasia Mutated (ATM) kinase is an essential checkpoint protein that is specifically activated by DNA DSBs and not by SSBs, even at numbers that relax chromatin supercoiling [12].
In this paper, we present a timing-robust model that preserves all the essential checkpoint conditions properly against timing variations.
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Interestingly, TTK, which is essential for checkpoint signaling [59], [60], is also directly affected by the mutational status of BRAF: TTK is destabilized when BRAF is depleted, but is stabilized by BRAF V600E, resulting in checkpoint hyperactivation [61].
As a first attempt to study SAC during the plant cell cycle, candidate A. thaliana orthologs of the human essential mitotic checkpoint complex proteins BUBR1, BUB3 and MAD2 were identified by OrthoMCL [13] clustering of orthologous proteins from six model eukaryotic species.
These phosphorylation events may directly recruit proteins essential for checkpoint activation to damage sites.
Partial reduction of essential mitotic checkpoint components in tumor cell lines caused mild chromosome mis-segregation, but no lethality.
A permissive role for FAK regulating proliferation and migration provides an essential adhesion checkpoint in cancer progression.
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