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The structural information obtained combined with functional data have led to models for receptor activation and desensitization by agonists, inhibition by antagonists and block of desensitization by positive allosteric modulators.
Examples to be discussed include mathematical models for receptor dynamics, pharmacokinetics, and metabolic and signaling pathway analysis.
These findings are consistent with models for receptor activation in which ligand-binding or T-ALL-associated mutations lead to conformational changes of the NRR that permit metalloprotease cleavage.
The relatively simple models for receptor internalization and recycling at high insulin concentrations and without insulin [ 34] were combined to describe receptor internalization and recycling at arbitrary insulin concentrations.
Similar(56)
Based on our current knowledge of how apoptosis is regulated, we describe here a new model for receptor induced cell death.
We next compare these data with our model for receptor aggregation and adaptor binding.
We begin with a toy model for receptor regulation and chemotaxis to illustrate the basic requirements for chemokine-driven oscillations.
This provided a very attractive and structure-based model for receptor activation control in which the intramolecular tether presents a barrier to spontaneous dimerization and activation [ 12].
Interestingly, we found that the formation of asymmetric kinase dimer is dispensable for ERBB3 phosphorylation by the activated EGFR kinase as well as the ERBB2 kinase thus revealing a novel model for receptor function.
We use the following parameters for the MWC model for receptor complexes: K a o f f = 0. 02 mM, K a o n = 0. 5 mM, K s o f f = 100 mM and K s o n = 1 0 6 mM [ 44, 47].
In summary, the work by Dang et al. provides a new model for receptor-mediated entry of picornaviruses into host cells that depends on the pH-triggered conformational change of the receptor molecule.
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