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. Author manuscript; available in PMC: 2009 May 8.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2009 Jan 22;29(4):539–547. doi: 10.1161/ATVBAHA.108.179937

Figure 2.

Figure 2

G2A is expressed by primary mouse hepatocytes. A, Morphological characteristics of primary hepatocytes isolated from high-cholesterol diet-fed (20 weeks) LDLR-/-G2A+/+ and LDLR-/-G2A-/- mice. B, Quantitative RT-PCR analysis showing G2A expression by primary hepatocytes (macrophages shown as positive control). The data shown is the average of 3 independent experiments, each performed in triplicate. Inset, Ethidium bromide-stained agarose gel showing the expected size of G2A-specific amplification products. 1: LDLR-/-G2A+/+ hepatocytes, 2: LDLR-/-G2A-/- hepatocytes, 3: LDLR-/-G2A+/+ macrophages, 4: LDLR-/-G2A-/- macrophages. C, Immunoblot analysis of G2A protein levels in hepatocytes and macrophages from LDLR-/-G2A+/+ and LDLR-/-G2A-/- mice. 1: LDLR-/-G2A+/+ hepatocytes, 2: LDLR-/-G2A-/- hepatocytes, 3: LDLR-/-G2A+/+ macrophages, 4: LDLR-/-G2A-/- macrophages. ERK2 immunoblot is shown as a control for protein loading.