Figure 1: RAR-independent, rapid activation of ERK1/2 by compounds 3 and 4. | Scientific Reports

Figure 1: RAR-independent, rapid activation of ERK1/2 by compounds 3 and 4.

From: All trans-retinoic acid analogs promote cancer cell apoptosis through non-genomic Crabp1 mediating ERK1/2 phosphorylation

Figure 1

(A) Structure of compounds. (B) Activation of ERK1/2 in Cos-1 assessed by western blot analyses under 100 nM for 30 min. Upper band depicts ERK1 (44 kDa) and lower band depicts ERK2 (42 kDa). (C) Compounds 3 and 4 do not activate RAR activity as detected by RAR reporter assay performed in Cos-1 cells treated with compounds at 250 nM for 24 hrs. (D) Pan-RAR antagonist AGN 193109 (100 nM, 1 hr pretreatment) fails to block rapid ERK activation in Cos-1 cells. Data (B–D) are representative of at least 3 independent experiments. (E) In vitro competition assay to displace 3H-atRA from Crabp1 by atRA, C3, and C4. Data is displayed as counts per minute (CPM). Asterisk shows significance: RA (p < 0.001), C3 (p = 0.023) and C4 (p = 0.014) versus control, and mean ± S.E.M (n = 4).

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