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Tregs secrete anti-inflammatory signals, inhibit macrophage migration, and induce noninflammatory M2-like macrophage differentiation (35).
These effectors suppress host defences, facilitate migration and induce the formation of the syncytium.
In keratinocytes, AGEs decrease cell viability and migration and induce the expression of proinflammatory mediators.
Moreover, self-assembling peptides can be functionalized with adhesion and signaling motifs to improve cell adhesion, proliferation, and 3D migration and induce cell differentiation [ 13, 14, 16].
For example, supernatants from S. aureus biofilms have been shown to reduce cellular migration and induce apoptosis in fibroblasts and keratinocytes [ 27, 39].
The activation of endothelial sst 1 may therefore inhibit cell migration and induce cytostatic effects in proliferating endothelial cells, without inducing apoptosis in quiescent cells.
Similar(49)
Compound 13 efficiently inhibited cell viability, cell migration, and induced G1 arrest.
Formin homology 2 domain containing protein (FHOD1), a mammalian formin, regulates cytoskeletal architecture, enhances cell migration, and induces gene expression from the serum response element.
Simulated weightlessness reduced cell size, disrupted microfilament, inhibited cellular proliferation and migration, and induced an increase in [Ca2+]i in MG63 human osteosarcoma cells.
EOPK significantly decreased HCT116 cell proliferation and migration, and induced G1 arrest without affecting normal cells.
Endostatin inhibits endothelial cell proliferation and migration and induces apoptosis [ 3- 5].
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