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The derived viral strains carrying the mutations exhibited a variety of distinct plaque phenotypes.
Indeed, 5-FU-resistant strains harboring these mutations exhibited decreased susceptibility to 5-FU.
More importantly, the 3D-differentiated neuronal cells expressing FAD mutations exhibited high levels of detergent-resistant, silver-positive aggregates of phosphorylated tau in the soma and neurites, as well as filamentous tau, as detected by immunoelectron microscopy.
Both RTs with 184V and 65R + 74V mutations exhibited similar processivity when compared with each other and a significantly decreased processivity as compared to WT RT.
Physiological characterization of each mutant demonstrated that the growth and metabolites accumulation properties of these mutations exhibited significant change upon pathway engineering.
When nicotine was used as an agonist, four mutations exhibited a statistically significant hypersensitivity to nicotine (S438D, S469A, Y576A, and S589A).
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Human males with these mutations exhibit precocious puberty while females do not have an obvious phenotype.
We find that the frequency of mutations exhibiting epistasis increases along the evolutionary pathway.
Mouse models with familial Alzheimer's disease (FAD) mutations exhibit amyloid-β-induced synaptic and memory deficits but they do not fully recapitulate other key pathological events of Alzheimer's disease, including distinct neurofibrillary tangle pathology4,5.
The aim of the present study was to determine whether South African PD patients with parkin mutations exhibit evidence for mitochondrial dysfunction.
Several allelic variants of the alpha1A pore-forming subunit of P/Q-type VDCCs have been described, and mice homozygous for these mutations exhibit gait ataxia, as do alpha1A knockout mice.
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