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Angiopoietin-like 3, present at extremely low levels in kidney, can bind integrin alpha-5/beta-3, whinducesucellcell adhesion and migration and regulates angiogenesis [41].
It stimulates endothelial cell proliferation and migration and regulates vascular endothelial cell growth factor expression in vascular smooth muscle cells (van Belle et al, 1998).
Taken together, our results are consistent with a model in which NEUROD2 expression is initiated in post-mitotic neurons right before the onset of migration and regulates a set of genes, that includes critical components of the Reelin pathway.
Specifically, the MMPs' action in the tumor microenvironment creates space for cancer cell migration and regulates their cell proliferation by proteolytical release and activation of the ECM-stored growth factors [ 114].
Furthermore, we show that type I collagen also promotes cancer cell proliferation, migration, and regulates apoptosis, in the same extent as type IV collagen, but that these two collagen types are expressed in different compartments of the tumor stroma in vivo.
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Using this system, we have demonstrated that expression of miR-328 reduced cell adhesion, aggregation, and migration, and regulated formation of capillary structure.
And some evidence points to a role for FN as a potential ligand for guiding radial neuronal migration and regulating the interactions between neurons and radial glia.
WNT/PCP signaling is thought to stabilize cellular polarity in epithelium of developing limbs, organize directional cell migration, and regulate directional cell proliferation (Wang et al., 2011).
FN is an important chemotactic protein for the storage of growth factors, along with its prolific interactions with cell surface molecules to facilitate cellular adhesion, migration and regulate cellular differentiation and proliferation [ 24].
MDA-Exo also contains a significant amount of mir-328, which has been shown to target CD44, reduce cell adhesion, enhances cell migration, and regulate formation of capillary structure [ 34].
Studies showed that, through several intracellular signaling pathways, activated ALK regulates cell proliferation, apoptosis, morphology, migration, and invasion, regulates tumor cell phenotype and mediates tumor cell transformation.
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