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. 2001 Mar;12(3):645–662. doi: 10.1091/mbc.12.3.645

Figure 6.

Figure 6

Overexpression of Git2-short, but not its GAP-inactive mutant, causes a redistribution of β-COP. HeLa cells were transiently transfected with 4 μg of pcDNA3 plasmids encoding HA-ARF1N126I (a and b), ARF6N122I (c and d), HA-Git2-short (e and f), the CA mutant (g and h), or 2 μg each of HA-Git2-short and myc-ARF1Q71L (i and j), using the calcium phosphate method. After 48 h, cells were fixed and HA-ARFs or HA-Git2-short proteins were visualized using mouse anti-HA antibody and Cy3 anti-mouse IgG (a, c, e, and g). Endogenous β-COP was visualized with rabbit anti-β-COP antibody and Cy2 anti-rabbit IgG (b, d, f, h, and j). In i, HA-Git2-short was visualized using biotin-labeled mouse monoclonal anti-HA antibody and Cy3 streptavidin (but shown in green), and myc-ARF1Q71L was visualized using monoclonal anti-myc antibody coupled with Cy5 anti-mouse IgG (shown in red). Each right column is of the same field as the left column, and arrows indicate cells overexpressing HA-ARFs (a–d), HA-Git2-short (e and f), or HA-Git2-short CA mutant (g and h), or both HA-Git2-short and myc-ARF1Q71L proteins (i and j). Focuses were adjusted 3.0 μm above the surface of the plates. Bar, 20 μm.