In contrast, CCL2- or CXCL7-neutralizing antibody treatment did not reduce either leukocyte adhesion (Supplementary information, Figure S5A) or endothelial ICAM-1 expression in CLP mice (Supplementary information, Figure S5B).
Precocious misexpression of Ddrdn using the Mesp driver inhibited this integrin-dependent TVC induction, thus supporting the notion that Ddrdn interferes with cell-matrix adhesion (Supplementary Figure 8).
Consistent with the observed downregulation of active Rac1 and Cdc42, MafB-depleted ECs showed significantly reduced directional migration in a 2D VEGF-A gradient as well as impaired collective migration and adhesion (Supplementary Fig. 4b d).
Interestingly, R-Yes-K− was unable to show this effect confirming c-Yes kinase-dependent signalling towards β-catenin and cell-cell adhesion (supplementary Fig. S7).
Treated cells showed very effective attachment, which revealed that combined treatments did not significantly affect cell adhesion (Supplementary Figure 3).
This revealed terms associated with angiogenesis, epidermal development and differentiation, taxis, proliferation and adhesion (Supplementary Table 2).
For the same disease and the miR-29 family members, the significant GO terms associated to the CCRCC profiles were extracellular matrix and focal adhesion (Supplementary Table 7).
As might be anticipated, consistently enriched GO terms were related to neuron development, axonogenesis and cell adhesion (Supplementary Material, Table S3).
Cells were seeded at a low density (2×10 viable cells/ml) in the absence of supplementary substrate or adhesion factors and let grow for one week under standard culture conditions.
In addition, hESC-PLTs adhered to and formed small aggregates on surfaces coated with fibrillar collagen type I under static conditions and treatment with a blocking anti-α2β1 integrin antibody inhibited this adhesion (Supplementary information, Figure S7).
Gene sets found to be enriched in Kras-specific genes included metabolism, signaling downstream of receptors, and adhesion (supplementary material Table S4), functions previously ascribed to mutant KRAS (Racker et al., 1985; Pollock et al., 2005; Rajalingam et al., 2007; Levine and Puzio-Kuter, 2010).
