The site specific mutants of the thermophilic P450 (P450 175A1 or CYP175A1) were designed to introduce residues that could act as acid base catalysts near the active site to enhance the peroxidases activity.
A tumor-specific mutant of the EGFR, EFGR variant III (EGFRvIII), causes constitutive activation of the receptor's tyrosine kinase activity and is frequently expressed in primary GBM (∼33%).
This suggests that the pro-fibrotic effects associated with this specific mutant of PPARγ in the presence of increased AngII levels are distinct from mechanisms driving cardiac hypertrophy at least under these experimental conditions, in contrast to previous studies.
This dual detection allows normalizing the abundance of one qTag (representing chromosomal DNA from one specific mutant) to the total number of all qTags (which corresponds to chromosomal DNA from all strains) present in the same reaction.
In order to investigate the role of multidrug efflux systems as bacterial defense mechanism, wild type and gene-specific mutants of the following bacterial species were analyzed: Erwinia amylovora 1189 (wild type), Escherichia coli TG1 (wild type) [ 22], Pseudomonas syringae DC3000 (wild type) [ 23] as well as the respective mutants with deletions in acrAB, tolC, or mexAB [ 24- 28].
Specific mutants of Tyr235 increase the Km for substrate (l-Trp) and lower Km for cofactor (BH4) [46].
Relative ligand-binding capacity (represented by binding %) to different mutants was calculated by the MS response of the ligand released from a specific mutant divided by the MS response of the total ligand present in the incubation sample.
The observation that ductal carcinoma-specific mutants of CK1ε promote the Wnt/Rac1/JNK and NFAT pathways and, on the other hand, inhibit the Wnt/β-catenin pathway are in good agreement with some clinical observations.
However, final titers qualify as a valuable measure for overall performance of a specific mutant strain over the whole course of the experiment.
Using specific mutants in the Walker boxes of RFS-1, which are compromised for stimulating strand exchange, we demonstrate that filament remodeling is critical for RFS-1/RIP-1 mediactivityivity.
The polymerase error frequency of a specific type of error (e.g., indel within the repeat or indel at a monitor locus) was calculated from the proportion of the specific mutants (among the total sequenced) multiplied by polymerase error frequency for each template.
