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The epidermal growth factor receptor (EGFR) T790M mutant is found in about 50% of clinically acquired resistance to gefitinib among patients with non-small cell lung cancer (NSCLC).
The MAH 4B2/ΔGPL mutant is found at significantly lower levels than the wild-type MAH strain within the intestinal tract of the worms.
When a mutant is found to show a defect in virulence, this method can also be used to determine at which stage of the infection process the defect occurs.
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After this treatment, one mutant was found which had lost its antagonistic property.
Thermal fluctuation of the mutant was found to be reduced upon PhC binding, which contributes to restoring its enzymatic activity.
The mutant was found also capable to produce MA from a guaiacol-rich true lignin hydrolysate, obtained from pine through hydrothermal conversion.
The R11E mutant was found to have activity near that of wild-type ImI, while R7L and D5N demonstrated activities reduced by at least two orders of magnitude.
The oncogenic potential of ALKF1174L has been the most studied, as this ALK mutant was found to exert potent oncogenic effects in both in-vitro and in-vivo models20.
Among the limited number of M2 mutants that confer amantadine resistance, the M2-V27A mutant was found to be the predominant mutant under drug selection pressure, thereby representing a high profile antiviral drug target.
Growth of the had1∆ mutant was found to be compromised at 38° or higher.
An important wheat male sterile mutant was found in 1972 by Gao (1987).
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