Sentence examples for models of inactive from inspiring English sources

Imatinib, dasatinib, sunitinib, CEP-701, and PKC-412, ATP-competitive small molecule inhibitors of type III receptor tyrosine kinases c-KIT and/or FLT3, were evaluated for binding to the closely related receptor, FMS, by docking into models of inactive and active conformations of the FMS kinase domain.

They achieve fine modulation in signaling specificity through adapting an ensemble of conformations rather than a two-state model of inactive and active states.

Sensitivity tests suggest that the problem is sufficiently serious to consider an alternative approach by either zonal modelling or explicit modelling of inactive turbulence effects.

To analyze the locus in its active state we used primary erythroid cells from fetal liver which were compared to fetal brain cells as a model of inactive loci.

Therefore, we have built comparative models of the inactive and active conformations of the three receptors based on the three GPCRs for which structures of both inactive and fully active conformations were available at the time of the study.

However to compare the models of the inactive and active conformations of the TSHR (as well as FSHR and LHR), the models should be produced based on templates of the inactive and active conformations of the same GPCRs.

In conclusion, to study activation of the GPHR TMDs, we built comparative models of the inactive and fully active conformations of their TMDs based on three GPCRs for which the crystal structures of both the inactive and fully active conformations were available.

Based on our experimental data, we have proposed molecular models of the inactive and the active Ron structure, which cast a new light on the mechanisms controlling Ron mediated signal transduction.

A "homology model" of the inactive conformation of Plk1 was constructed, as the crystal structure in its inactive conformation is unknown.

In addition to the blocking segments, a cluster of hydrophobic amino acid residues centred about Val appears to stabilize the inactive conformer, and a substitution of a glutamate residue for Val in the model of the inactive procaspase-3 suggests a mechanism for activation resulting from the mutation.

The design of analogues was guided by the docking of potential compounds into a model of the inactive form of GPR55.