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Mutation of these sequences unveiled a complex regulatory mechanism since not all mutated boxes showed increased promoter expression.
Mutation of these proline residues to alanine stabilises the protein.
Mutation of these cysteines also compromises GREUL1's ability to induce cement gland.
Mutation of these sites has no effect on the phosphorylation of Chk1 by ATR.
Mutation of these hydrophobic residues in PX5 (Y132A, L133A or F136A) abolishes its binding with IncE (Figure 2d).
Mutation of these sites inhibited transcription activation and abrogated the transcriptional response to ERK1/2.
Mutation of these serines to alanine, either alone or in combination, inhibited the ability of Raf to induce paxillin phosphorylation.
The mutation of these residues resulted in the changes of the structure stability and the reduced or absence catalytic activity.
Mutation of these residues led to a significant decrease in Rab9 binding, but did not alter the global folding of the protein.
Thus, our failure to detect an effect of Homer2 deletion upon binge alcohol intake using SHAC or DID procedures could very well relate to the apparent 'resistance to mutation' of these models (see Blednov et al, 2012).
The back mutation of these residues to the corresponding chicken residues completely recovered the pT231-peptide binding affinity and specificity of the humanized antibody.
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