Sentence examples for migration by activation from inspiring English sources

The NCAM and L1 family of adhesion molecules are thought to trigger neurite outgrowth, axonal growth or cell migration by activation of a number of signal transduction pathways, including PLCγ-, PI3K-, Erk- and PKA-dependent pathways [7], [39].

Interaction of GRO α/CXCL1 with its receptor CXCR2 promotes cancer cell invasion and migration by activation of cellular AKT/NF- κB signalling (Kuo et al, 2012).

Monocyte chemotatic protein 1/CCL2, through interaction with its receptor CCR2 on cancer cells, increases cancer cell invasion and migration by activation of protein kinase C and protein tyrosine phosphorylation (Monti et al, 2003; Chiu et al, 2012).

TNK2 was suggested to regulate Cdc42-driven migration by activation of breast cancer antioestrogen resistance 1 (BCAR1); however, distinct from this effect is evidence for a role of TNK2 in the regulation of epidermal growth factor receptor (EGFR) endocytosis and degradation.

Because Akt1-mediated effects on PC3 cells can be reversed upon modulation of integrin β3 affinity either using blocking/activating antibodies or expression with inactive mutant of integrin β3, our data demonstrate that enhanced prostate cancer cell migration and transendothelial migration by Akt1 activation is mediated through inside-out activation of integrin αv β3.

A quantitative analysis in Fig. 2D showed that induced cell migration by synthetic activation of PI3K is statistically highly significant (p<0.0001), while endogenous activation of Rac does not cause a significant increase in cell migration.

A recent report on T47D breast cancer cells showed that genistein induced transcriptomic and proteomic signatures that indicate rapid cell growth and migration by dynamic activation of cytoskeleton remodeling in the presence of ERα only [ 14].

Not only is the MAPKAPK2/Hsp-27 pathway a promising potential target for therapeutic intervention, but the isoflavone genistein, an oestrogen analog and candidate chemotherapeutic agent, inhibits cell migration by blocking activation of this pathway (Xu and Bergan, 2006), emphasising the validity of this proposed therapeutic approach.

These results suggest that BBP promotes cell migration and invasion by activation of AhR/Gβ/PI3K/Akt/NF-κB signaling.

Investigations in the breast cancer cell line MCF-7 showed that miR-21 is responsible for migration and invasion by activation of the epithelial-mesenchymal transition (EMT).

In line with the fact that activation of these pathways is known to promote malignancy of cancer cells, it could be demonstrated that TRAIL stimulation can enhance migration and invasion by activation of these pathways.