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. Author manuscript; available in PMC: 2017 Jan 17.
Published in final edited form as: Sci Signal. 2016 Jul 26;9(438):ra76. doi: 10.1126/scisignal.aaf0791

Fig. 6. SIRT1 production was lower in Syx−/− EBs and was partially inhibited by RhoA.

Fig. 6

(A) Immunoblot showing SIRT1 abundance in dissociated Syx+/+ or Syx−/− EBs at the indicated time points (one of two independent experiments). GAPDH is a loading control. (B) Immunoblot of cells from dissociated RA-treated Syx−/− EBs after transfection by GFP–CA-RhoA and GFP–wild-type RhoA (one of two independent experiments). (C) Immunoblot showing the effect of SIRT1 transfection on RARγ production in cells dissociated from RA-treated EBs (two-sample t test, equal variance, mean ± SD, n = 3 independent experiments, P = 0.01). (D) Immunoblot showing that transfection of cells dissociated from RA-treated Syx+/+ EBs with SIRT1 increased SMAD1 phosphorylation (pSMAD1) and reduced the abundance of the neural differentiation markers Tubβ3 and vimentin (one of two independent experiments). (E) Effect of SIRT1 coexpression with Noggin or Rarγ on SMAD1 phosphorylation in 8-day EBs transfected by the indicated plasmids (one of two independent experiments; the left lanes were immunoblotted on a separate membrane). (F) Signaling scheme representing the data shown in (A) to (E). Solid lines represent direct regulatory events, whereas dashed lines represent events that either are indirect or have not been shown to be direct.