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. 2011 Sep 21;6(9):e24194. doi: 10.1371/journal.pone.0024194

Figure 6. KGFR-mediated early differentiation is independent on PLC-γ recruitment and activation.

Figure 6

(A) HaCaT cells transiently transfected with KGFR WT, with KGFR Y769F signaling mutant or with KGFR Y656F/Y657F kinase dead mutant were treated with TG as above. Quantitative immunofluorescence analysis performed as described in figure 2D shows that, similarly to KGFR WT, KGFR Y769F overexpression significantly increases the percentage of cells expressing K1 either in TG-treated and in the control cells, while the KGFR Y656F/Y657F overexpression does not affect it. Results are expressed as mean values ± SE. Student's t test was performed and significance level has been defined as *p<0.001, **p<0.01, ***p<0.001 and ****p<0.05 vs the corresponding surrounding cells that do not display KGFR overexpression. Bar, 10 µm. (B) HaCaT cells were transfected and treated with TG and KGF as above. KGFR mRNA (left panel) and K1 mRNA (right panel) transcript levels were quantitated by real-time RT-PCR: a ligand-dependent increase in K1 mRNA expression is observed in cells transfected with KGFR WT and with KGFR Y769F but not in cells transfected with KGFR Y656F/Y657F. A ligand-dependent down-modulation in KGFR mRNA expression is observed in HaCaT KGFR WT cells and in HaCaT KGFR Y769F cells but not in KGFR Y656F/Y657F cells. Student's t test was performed and significance level has been defined as *p<0.001, **p<0.05, ***p<0.005 and ****p<0.001 vs the corresponding unstimulated cells.