Sentence examples for mutation we created from inspiring English sources

Figure 3Bii and Figure 3Cii shows the mutation we created on the binding sites of the 3'UTR of both Bambi and Crim1.

To evaluate the 3D impact of the mutation, we created a homology model to compute and compare mutant and wild-type structures.

To support the interpretation of putative kinase domain mutations, we created a prototype mutation interpretation tool for tyrosine kinases (TKs), called "Mutagrator", located at http://cbio.mskcc.org/∼lash/mutagrator/ (freely available to the research community).

To evaluate the level of WGA artifact mutations we created small colonies, each founded by a single RMA cell [18], and analyzed the cell identifier for each progeny cell (using the same set of MS loci).

For each possible pair of mutations, we create a regular expression by using the wildtype residues and the distance between them; for two normalized mutation mentions w1 N1 m1 and w2 N2 m2, sorted in the ascending order of N i, the regular expression will be w1 { N2 – N2 – 1} w2.

We then evaluated whether the mutations that we created in pla1, rna15 and pab2 could suppress meiotic arrest in sme2Δ cells.

The specific rules are: 1. Mutation: First, we create a "mutant" vector v j (t) by perturbing a parental parameter vector x j (t): v j (t ) = x j (t ) + F · d j (t ).

To determine the effect of p.S466L mutation on serum tHcy, we created two genetically engineered mouse strains.

In order to analyse the most common mutations in human tumours, we created a Fbxw7 fl(R482Q /+ mouse and conditionally expressed this mutation in the intestines using Vill-Cre.

To elucidate the functional requirements for activation of the MEKK1-dependent apoptotic pathway, we created mutations within MEKK1.

To determine if calpain cleavage could also play a role in SMN stability, we created mutations in the C-terminus of EGFP-SMN and assayed their susceptibility to endogenous calpains.