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A number of molecular interactions triggered by EGFR activation have been characterized in HNSCC.
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The scope of our model is limited to the chain of molecular interactions that are triggered by the inducers, which are then forwarded through the phosphorelay, ultimately leading to the activation of the master regulator Spo0A, and to the expression of the spoIIA, spoIIE and spoIIG genes.
The results described in this study characterized the immunogenicity of EnvBF in the Balb/c model, although cross-reactivity of murine T cells does not directly translate to humans, the underlying principles of the molecular interactions involved in triggering T cell responses are the same in both species.
A detailed mathematical implementation of all downstream molecular interactions that ultimately trigger cytotoxic response will reduce the generality and simplicity of our model, so we consider this approach far from the scope of this contribution.
Importantly, the goal of this research was to test molecular docking as a computationally inexpensive virtual screening approach for the reliable prediction of critical drug HLA-B*57 01 drug HLA-B*57 01ggerinteractionstriggering
Results consistently echo whole cell-cell behavior [20], [21], [22], supporting the validity of this approach for both dissecting the link between surface molecular interactions and T-cell triggering, and developing efficient artificial T-cell activation strategies.
It was therefore possible that the calcium elevation was triggered by molecular interactions between cell-surface components, such as ligands and receptors, of individual cells from the heterogeneous tissues.
On the other hand, the expression of resistance genes in the infected host is also triggered by specific molecular interactions to combat the infection.
Ligand and receptor induced molecular interactions on the plasma membrane trigger a signaling cascade that culminates into specific gene expression.
These changes are initiated by sequence-specific events, which trigger a cascade of molecular interactions resulting in feedback mechanisms, alterations in chromatin structure, histone posttranslational modifications (PTMs), and ultimately establishment of distinct transcriptional states.
Collectively, these data support the view that (1) one or several distinct molecular interactions with the host cell surface specifically trigger the RON complex secretion, and (2) a one-shot secretion is used for junction assembly into the host cell PM.
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