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. 2017 Feb 3;8(16):27034–27046. doi: 10.18632/oncotarget.15067

Figure 4. Cells growth is decreased by gC1q.

Figure 4

Cellular growth of HT29 cells transfected with the wild type (wt) or the deleted (Δc) α4 integrin chain and plated on collagen type I (Coll I), EMILIN1, or gC1q expressed as either normalized cell index A. or doubling time B. and calculated as the mean ± SD from n = 3 experiments with n = 6 replicates. Cells were allowed to proliferate for 48 hours. Cell index curves were then normalized (normalized cell index) to the point corresponding to 1 hour after plating (maximum cellular adhesion) in order to express proliferation ability independently from attachment to a particular substrate. C. HT29 cells transfected with the wild type (wt) or D. the deleted (Δc) α4 integrin chain and plated in 0.4% agar in the presence or in the absence of gC1q. E. Modulation of HRas-Ub and pERK1/2 in α4 integrin chain transfected HT29 cells. HT29 cells were lysed 24 hours after plating on collagene type I (Coll I) or gC1q coated plates. The blots were incubated with the indicated antibodies (see under Material and Methods). Tubulin was used as loading control. Cell lysates were pulled down on a Raf-GST resin to isolate HRasGTP-Ub.