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. 2015 Sep 24;26(2):166–180. doi: 10.1093/glycob/cwv084

Fig. 5.

Fig. 5.

Rab prenylation inhibitor replicates statin effects on GSLs. (A) Scheme for effect of statins or specific inhibitors of farnesyl transferase, geranylgeranyl transferase −1 or geranylgeranyl transferase II on protein prenylation. (B) Effects of specific prenylation inhibitors on GSL and GCS expression were determined. The Rab geranylgeranyl transferase inhibitor, 3-PEHPC, was effective to increase GlcCer (TLC, upper panel) and GCS (western blot, lower panel). ACHN cell treatment was 48 h with 3 mM 3-PEHPC, 15 µM FT1-277, 10 µM GGTI-2133 or 20 µM rosuvastatin. Inhibition of prenylation by 3-PEHPC and FTI-277 are indicated by appearance of the slower migrating, unprenylated forms of Rab6 (25 kD) and the co-chaperone HDJ2 (40 kD), respectively. Inhibition of GGTase I is confirmed using an antibody specific for unprenylated Rap1A (21 kD). Blots were probed with anti-GAPDH to verify equal sample loading and transfer. (C) Neutral GSLs of A431S cells treated with the inhibitor panel as in (A). A dose–response between 0 and 10 µm lovastatin was seen for GlcCer and Lc3Cer elevation and 1 mM 3-PEHPC caused similar increases within this range. (D) Lc3CerS enzyme activity in lysates of A431S cells treated as in (B). Band intensity (arbitrary units) of NBD-Lc3Cer was quantified using Image J; error bars represent the range of duplicate samples divided by two. This figure is available in black and white in print and in colour at Glycobiology online.