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Ultraviolet (UV) rays damage a key gene in skin cells involved in fighting off tumors, and at the same time appear to help these dangerous mutant cells survive sun exposure, says a report in the 26 November issue of the Proceedings of the National Academy of Sciences.
Homozygous null mutant cells survive only briefly in culture and in proliferating tissues, such as bone marrow, and are rapidly replaced by heterozygous null mutant cells.
We chose the thermosensitive cut3-477 mutotion to weaken condensin because this mutation in the Cut3/Smc4 ATPase has been shown to cause synthetic lethality when combined with top2-250 athehe permissive temperature of 30° (Saka et al. 1994), suggesting that cut3-477 mutant cells survive with a partly defective condensin complex.
Based on the observation that about 1% of polymyxin B-sensitive B. cenocepacia heptoseless LPS mutant cells survive treatment with 500 μg/ml of the antimicrobial peptide polymyxin B for 24 hours (Loutet and Valvano, unpublished), we hypothesized that B. cenocepacia heptoseless LPS isolates with increased resistance to polymyxin B could be obtained.
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However, in liver tissue, null mutant cells survived well and even after two weeks still 95% of this organ consisted of null mutant cells [8].
Only 69±16%6% of the mutant cells survived, compared with 94 ± 12% surviving wild type cells.
In addition, malignant tumorigenesis requires a permissive tissue environment in which mutant cells can survive, proliferate, and express their neoplastic phenotype.
This allows mutant cells to survive under severe heat stress, such as exposure to 48°C for 3 h.
In engulfment-deficient mutants, a significant fraction of those cells survive and remain alive during adulthood (Supplementary Figure S7).
However, rapamycin cannot extend the chronological lifespan (i.e., the time post-mitotic cells survive during the stationary phase [ 78]) of yeast mutants that lack functional Atg1, Atg7 or Atg11 [ 79].
However, these cells survive poorly after passage.
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