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It is known that cancer lineages have the ability to avoid the normal checkpoints of cellular regulation to empower longevity [83, 84].
However, as opposed to a typical differentiated cell, the more flexible cancer cell, in the absence of normal checkpoints, utilizes an invigorated form of reverse evolution for coping with epigenetic stresses.
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*Green, which the great majority of passengers will receive, means you can head for your flight simply by passing through the normal checkpoint inspection.
In fission yeast and metazoans, the normal checkpoint response to damage during G2 is a cell-cycle arrest due to inhibition of CDK [reviewed in [22]].
Red-Br-nos-induced downmodulation of MT dynamicity in healthy cells may be harmless because normal checkpoint systems mitigate the impact.
The accumulation of FA cells with a 4N DNA content and CHK1 hyperphosphorylation could be the consequence of a normal checkpoint response in cells with DNA damage hypersensitivity (41).
These include the rapid exploration of its environment through flexible phenotypic shifts, unusual longevity, re-connection with its evolutionary path, and its singular capacity to elude the normal cellular checkpoints that constitute the regular orderliness of cellular life.
Its privileges are a product of its malleability through the absence of normal cellular checkpoints with a concomitant ability to slide backwards with some flexibility along an evolutionary scale since it maintains a connection to its evolutionary problem-solving capacity.
In normal cells, checkpoints in the cell cycle play an important role of guiding normal cell cycle while in cancer cells, disruption of the checkpoints is responsible to abnormal growth of cancer cells.
Primary Ctrl fibroblasts displayed a normal G1/S checkpoint arrest, in contrast to A-T fibroblasts in which this checkpoint defect resulted in a significant increase in the percentage of G2 phase cells.
Not only are these proteins required for normal spindle checkpoint function [28] [30], but in fission yeast we have shown that Mad3p is even required for the overexpression of Mad2p to induce a metaphase arrest [31].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com