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. 2010 Dec 21;39(8):3224–3239. doi: 10.1093/nar/gkq1289

Figure 6.

Figure 6.

Silencing of the Arxes abrogates adipogenesis, while Spcs3 knockdown does not change adipogenic marker gene expression. 3T3-L1 cells were transduced with silencing constructs (siArxes or siSpcs3) or nontargeting control (ntc), and induced to undergo adipogenesis with standard DMI treatment unless indicated otherwise. (A) qPCR mRNA measurement shows that Arxes knockdown using the siArxes silencing constructs is specific to the Arxes, while Spcs3 expression is not reduced. Data are presented as mean ± SEM from three independent transduction experiments. (B) Lipid droplets were visualized by oil red O staining of 7 days differentiated 3T3-L1 cells. Lower panel of the oil red O staining shows a partial rescue of the differentiation deficiency if 1 µM rosiglitazone is present during differentiation procedure. (C) Expression of marker genes of adipogenesis was measured with qPCR on Day 7 of adipogenesis in Arxes-silenced and control cells. Data are presented as mean ± SEM from three independent transduction experiments. (D) qPCR mRNA measurement shows that Spcs3 knockdown using the siSpcs3 silencing construct is specific to the Spcs3 while Arxes mRNA is not reduced. Data are presented as mean ± SEM from two independent transduction experiments. (E) Spcs3 knockdown does not influence adipogenic marker gene expression as measured with qPCR on Day 7 in DMI induced cells. Data are presented as mean ± SEM from two independent transduction experiments.