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Fig. 7. Overexpression of RGS19 protein attenuates Wnt3a-induced formation of PE. (A) F9 cells transiently transfected with vectors encoding Fz1, or Fz1 and RGS19, were treated with or without Wnt3a or retinoic acid (RA) for 5 days. Lysates were collected and separated by SDS-PAGE on an 11% acrylamide gel, transferred to nitrocellulose and probed with an antibody against cytokeratin endo A (TROMA), a specific marker for PE formation. Cells expressing only Fz1 were able to differentiate upon Wnt3a stimulation, whereas those containing both Fz1 and RGS19 were not able. RGS19 was unable to block PE formation induced by RA treatment. The results displayed are from a single experiment representative of more than three independent tests. (B) Bands from multiple experiments were quantified by densitometry. Results are displayed as the `fold change' in cytokeratin endo A expression as compared with untransfected control. The data shown are mean values (±s.e.) of at least three separate experiments. *P<0.05 for the difference between untreated cells and those treated with either Wnt3a or RA. (C) F9 cells transiently transfected with RGS17, RGS19 or an empty vector were treated with or without Wnt3a for 4 days. Cells were stained with an antibody against cytokeratin endo A and imaged by indirect immunofluorescence. Wnt3a treatment induced cytokeratin endo A expression in cells transfected with the empty vector or one encoding RGS17. Overexpression of RGS19 blocked cytokeratin endo A expression. IF, immunofluorescence; OE, overexpression; PC, phase contrast.
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