Even with a 10-fold input advantage, the 3D-G64S virus was unable to compete with 3D wild-type virus in the context of the revertible attenuating mutation; however, in the context of a non-revertible version of the 2C-F28S attenuating mutation, 3D-G64S virus matched the replication of 3D wild-type virus.
Inactivation may be due to a specific reason such as a mutation, however in the case of myosin motility we observe it in all samples, so the inactivation is probably a result of protein damage.
Converse to this harmless effect of simple mutations, however, in silico modeling suggests that simultaneous mutation is lethal for phenotype in cancer cell growth, a finding that agrees with already published reports.
It is estimated that, in common adult epithelial tumours, there are on average 5 7 driver mutations; however, in haematopoietic malignancies this number might be lower (Stratton et al., 2009).
This mutation, however, results in a missense mutation, W460X.
No second mutation, however, was identified in NEB and this nonsense mutation likely has a modifying impact on the phenotype of the patient.
The mutation, however, was not situated in a known neutralizing epitope [ 43, 44].
The mutation, however, was not found in 200 healthy Han Chinese controls.
Other mutations, however, result in a loss of function in the gene they affect.
Unlike SOS1 mutations, however, those in SOS2 are restricted to the DH domain.
Many such mutations, however, occur in genes that encode for proteins of unknown function, which limits our molecular understanding of, and ability to devise treatments for, human disease.
