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The mutations of these genes are now believed to play a key role in the creation of cancer.
It is not clear whether spontaneous cardiomyopathies are associated with random genetic mutations of these proteins.
Mutations of these receptors can lead to tumorgenesis (Cooke 2000).
Mutations of these three amino acid residues render the peptide completely ineffective against CHPV.
Mutations of these residues, S166A, Y181A, Y181F, and K185A, resulted in a complete loss of activity (Table 2).
Point mutations of these hydrophobic residues impaired the DAXXDHB-ATRXDBM interactions, and a DAXX double mutant (F87A/Y124A) completely lost its ability to bind to ATRX (Fig. 2C).
Members of the human Nav channel family share high sequence similarity and mutations of these Nav channels are known to cause a vast variety of channelopathies.
Mutations of these susceptible genes, together with sensitive endpoints, could be used to evaluate TiO2-NPs toxicity at the concentration of 0.0001 μg/L.
Thus, it is tempting to speculate that mutations of these two residues may affect the local mobility or protein-protein interactions; however, future studies are necessary to confirm this speculation.
The sun's rays will cause mutations of these chemicals, making them even more harmful.
But certain mutations of these genes can dramatically raise cancer risk.
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