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Studies in bacteria and yeast imply mutator mutations confer a selective growth advantage on cells harboring these acquired mutations [ 24, 25].
If mutations confer a proliferative advantage, mutated cells can bypass the in vitro lifespan limit and rapidly replace the existing population [ 14, 15].
The mutations confer a selective advantage to myeloid progenitors at the expense of lymphoid progenitors.
As discussed above, whether these mutations confer a cellular fitness advantage should be dependent on the state of the neighborhood (competing cells and the state of the niche).
Background & Aims: Whereas it has conclusively been demonstrated that biallelic MutY human homolog (MYH) mutations confer a significant risk for colorectal cancer (CRC), the influence of monoallelic mutations remains controversial.
Biophysical studies and long-timescale molecular dynamics experiments reveal the mechanisms by which ten point mutations confer a 35,000-fold enhancement in binding affinity, and offer atomic-scale views of the role of conformational dynamics in PD-1/PD-L1 interactions.
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Like somatic mutations, most CFC germline mutations confer an increased kinase activity, while some are kinase impaired.
SOD1 is ubiquitously expressed and the mutations confer an unidentified toxic property on the enzyme [3], [4], [5].
Intragenic RUNX1 mutations confer an adverse prognosis in AML.
Results suggest that protein-truncating BRCA2 mutations confer an elevated RR of early-onset prostate cancer.
24 These mutations confer an increase in the lipid kinase activity of PI3k, indicating gain-of-function mutations that result in active signaling.
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