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. 2018 May 11;293(25):9759–9769. doi: 10.1074/jbc.RA118.002743

Figure 1.

Figure 1.

RSPO1–4 have differential dependence on LGR4 to potentiate Wnt/β-catenin signaling. A, upper panel, WB of LGR4 and actin in parental STF cells (P) and two clones (C6 and C11) with CRISPR-mediated KO of LGR4. Lower panel, WB of phospho-LRP6 (pLRP6), total LRP6 (tLRP6), and actin in parental and STF-LGR4KO C11 cells treated with RSPO1 and Wnt3a-CM for 5 h. Ratios of phospho-LRP6 and total LRP6 to actin, normalized to parental STF without RSPO1 treatment, are shown below the WB bands. B, TOPFlash results of RSPO1 response in parental STF cells and LGR4KO C6 and C11 cells. C, TOPFlash results of RSPO1–4 in parental STF cells. D, TOPFlash results of RSPO1–4 in STF-LGR4KO C11 cells. All TOPFlash activity (Act.) was normalized by the cell number first and then to the baseline (no ligand, Wnt3a-CM only). All error bars are S.E. (n = 3).