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Defining the kinetics of orexin signaling is fundamental for understanding normal neurobiology, especially in relation to variations in arousal and sleep/wake regulation.
Initial studies, aimed at defining the kinetics of PI3K/mTOR and canonical Smad signaling in pHLFs during TGF-β1-induced collagen deposition, revealed that Smad signaling was rapid and relatively short-lived with Smad2 phosphorylation peaking within the first hour and declining after 2 h (Fig. 1a).
These studies indicate that a single cluster of hydroxy amino acids within the C-terminal seven amino acids of the orexin-1 receptor determine the sustainability of interaction with beta-arrestin-2, and indicate an important role of beta-arrestin scaffolding in defining the kinetics of orexin-1 receptor-mediated ERK MAPK activation.
In previous Steered MD studies of the unfolding of titin, it was that found that hydrogen bonding with explicit solvent waters plays a key role in defining the kinetics [23] [24].
Thus, KIAA1524/CIP2A may be essential in defining the kinetics of the subsequent PP2A-mediated deactivation of the MTORC1 substrates.
Defining the kinetics of cellular responses to taxol-induced stress in terms of checkpoint activation, cell-cycle arrest, and apoptosis will contribute to a coherent view as to how different agents with different cellular targets may be combined with taxol to enhance therapeutic effectiveness.
Similar(54)
A critical developmental switch defines the kinetics of kidney cyst formation after loss of Pkd1.
Additionally, attempting to define the kinetics of changes in gene expression by sequential sampling is pragmatically unrealistic.
We describe a novel method to directly assay CPP-mediated delivery of peptide cargo into the cytosol, and use this method to define the kinetics of this process.
The Pitzer ion interaction model and the Freundlich non-equilibrium isotherms are utilized to define the kinetics of salt crystallization/dissolution.
We have defined the kinetics of neuron-specific BAF complex assembly in the formation of induced neurons from mouse embryonic stem cells, human fibroblasts, and normal mouse neural differentiation and, using proteomic analysis, found that this switch also includes the removal of SS18 and its replacement by CREST at mitotic exit.
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