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b The EGFR-T790M mutant is known to be responsible for resistance to erlotinib and gefitinib, and their docking scores decreased by 20 and 36%, respectively, in the docking simulation.
The elo3Δ mutant is known to cause the aberrant trafficking of the essential plasma membrane proton pump protein Pma1 [32].
Overexpression of the Rab5Q79L mutant is known to promote homotypic endosomal fusion [53], [60], resulting in the formation of large endocytic structures that fulfill the size criterion of macropinosomes.
In fact, the MGM101 null mutant is known to display the petite phenotype [ 42] due to loss of mitochondrial DNA.
This mutant is known to have a longer photocycle (∼10 s) but retains an ability of proton pumping.
A mutated version of a protein called lamin A causes HGPS; this mutant is known as progerin.
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The ability to evolve robust mutants is known to depend on the network architecture.
At variance with the great majority of protein kinases that become active only in response to specific stimuli and whose implication in tumors is caused by genetic alterations conferring to them unscheduled activity, the highly pleiotropic Ser/Thr-specific protein kinase CK2 is constitutively active even under normal conditions and no gain-of-function CK2 mutants are known.
Several long-lived mutants are known which predominantly or exclusively respire via AOX.
In mouse, mutants are known for both the ligand, Eda-A1 (Tabby), and the receptor, Edar (Downless).
For example, two TS lethal mutants are known to affect protein synthesis by impairing ribosome function [9], [10].
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