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The TNF-α then acts upon LCs in a paracrine fashion to provide a second stimulus for migration.
However, the migration is inhibited more strongly in NOBEC expressing ecto-ErbB4, supporting the hypothesis that this soluble fragment, binding to NRG1-typeIII, leads to the production of a cytoplasmic fragment responsible of the stimulus for migration.
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It is suggested that endothelial cells must exhibit a phenotype of non-directional motility as a prerequisite for responding to stimuli for migration.
The impact of C5a on HSC migration was nearly as robust as PDGF, known to be a potent stimulus for HSC migration.
The central Asian horse-riding Scythian culture expanded, and an increased population density was a stimulus for westward migration towards southeastern Europe.
Antagonism of TLR7 and TLR9, however, does not impact the inflammatory cell infiltrate, suggesting that the stimuli for cell migration are separate from the stimuli for cytokine production.
It has been well established that Ang II is a potent stimulus for vascular SMC migration [5], [6], [8], [10], [30].
These results emphasise the importance of a redox threshold in stromal cells needed to sustain a stimulus for epithelial cell migration.
Several in vitro studies have indicated that activation of ErbB receptors is a potent stimulus for survival, proliferation, migration, and invasion of PCa cells.
According to this view, angiogenic factors produced by the tumour may principally function to induce the initial stages of endothelial cell activation and migration into the stroma, and to provide a chemotactic stimulus for the subsequent directed migration of the resultant sprouting cells toward the tumour.
This is because elongation is the stimulus for cell proliferation and migration; without it, the cell may migrate to an extent, but will not proliferate until stimulated.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com