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Since reduced-activity mutants could still activate MEK/ERK via CRAF [ 11, 13, 14], demonstration of mutant-induced MEK or ERK phosphorylation in cell culture systems without evidence of inhibition of mutant-induced MEK or ERK phosphorylation by BRAF inhibitors was not sufficient to define a kinase-activated mutant.
It is hoped that this model would have the capability to provide a clear demonstration of the mutant selection window in vivo and support arguments for how antimicrobial dosage regimens adjustment could severely restrict the amplification and enrichment of resistant mutant for cefquinome.
These patient-related findings were preceded by the experimental demonstration that expression of mutant K14 in transgenic mice causes abnormalities similar to EBS (Vassar et al. 1991).
This observation is consistent with our previous demonstration that expression of mutant ezrin Y477F does not inhibit growth in three-dimensional cell colonies or primary tumour xenografts [ 12].
The demonstration of copy-up mutants in spite of multiple mechanisms of replication regulation [23] implies that the molecular mechanisms of replication regulation are not infallible and therefore unable to explain the evolutionary stability of copy numbers.
This is the first demonstration that mutant IFITM5 is expressed in human bone.
To our knowledge, this is the first demonstration of a transdominant Tat mutant that targets multiple, distinct steps in the HIV-1 replication cycle: proviral gene transcription, Rev-dependent mRNA transport and reverse transcription.
Despite the demonstration of CMA blockade by mutant ASYNs in the in vitro assay with purified proteins and isolated liver lysosomes, it remains unclear whether such blockade can be conferred in a cellular context, and whether it could be responsible for the lysosomal dysfunction that has been observed in certain instances when ASYN is overexpressed.
The relevance of these approaches has recently been demonstrated by the demonstration of a marked early reduction in F-FDG uptake in BRAF mutant melanoma using the novel BRAF inhibitor, vemurafenib [ 53].
Our results serve as the first demonstration of the identification of soybean mutants controlling seed phenotypes discovered through the reverse genetics technique TILLING.
The ΔglcD1 mutant allowed the demonstration of enhanced carbon flux into the glycolate pool after a shift to lowered Ci during the chase phase (Figure 3).
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