Sentence examples for mutation of three from inspiring English sources

Exact(13)

Notably, it was shown that the triple mutation of three phosphorylation sites to Asp can somehow mimic the phosphorylation of these three sites in cells (Suijkerbuijk et al., 2012).

In addition, separate mutation of three conserved residues Pro49, Pro52 and Lys54 – they are required for peptide recognition by SH3 domain –– in a designed peptide to Ala would completely abolish the capability of this peptide activating TIM.

Mutation of three additional SIR2 homologues, nst-2, nst-3 and nst-5, partially relieved silencing.

Stabilization of MdmX by mutation of three serine residues to alanines (Mdmx Ser 341, Ser 367 and Ser 402) dramatically decreases p53 activity and increases reprogramming efficiency [ 126].

Mutation of three hydrophobic residues, Leu171Arg, Gln175Arg and Phe179Arg, resulted in insoluble protein that was found in inclusion bodies, underscoring the important role these residues have in dimerization and hence proper protein folding (Supplementary Figure S1A B).

Mutation of three putative phosphorylation sites in the Bak α4-helix also failed to support a role for phosphorylation within the hydrophobic binding groove in regulating Bak apoptotic function.

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Similar(47)

Mutation of two putative phosphorylation sites in the N-terminus of KCNQ1 and one site in KCNE1 (S102) blocked the inhibition of Ang II.

Mutation of two of the sites, S324 and T515, partially inhibited the ability of muskelin to self-associate in cells and inhibited responsiveness to activated PKC.

In rel2 mutant, the mutation of two nucleotide substitutions in DUF630 domain led to the loss-of-function of REL2 locus and the function of REL2 could be confirmed by complementary expression of REL2 in rel2 mutant.

However, the mutation of two nucleotide substitutions in the ORF region causing amino acid substitutions (Cys3 to Tyr3, Val14 to Met14) should lead to loss of REL2 function in the mutant.

A mutation of one of the 70 genes its function in giraffes still unknown causes defects to both bone and cardiovascular development in humans and mice.

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