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. Author manuscript; available in PMC: 2012 Mar 20.
Published in final edited form as: Mol Carcinog. 2010 Dec 10;50(5):319–333. doi: 10.1002/mc.20707

Figure 8.

Figure 8

Subcellular localization of AC proteins in VILIP-1-negative CC4A, CH72T3 and VILIP-1-positive CC4B, CH72 SCC cells. A. Images from confocal immunofluorescence microscopy of CC4A and CC4B cells using AC-comm antibody against all AC isoforms were analyzed in Image J (outer rings show whole cell area, outer minus inner rings show membrane areas used for quantification). B. Quantitative analysis of the signal intensity of AC fluorescence show that the whole cell fluorescence intensity, as well as intensity at the cell surface membrane is significantly increased in VILIP-1-positive cell lines CC4B and CH72 compared to more aggressive VILIP-1-negative cell lines CC4A and CH72T3 (p< 0.0001, p< 0.001, N = 3, n > 28). Error bars indicate standard deviations. C. Relative fluorescence intensity (ratio of surface and whole cell fluorescence). D. Western blot analysis using AC-comm antibody against all AC isoforms in VILIP-1-positive cell lines CC4B and CH72 compared to more aggressive VILIP-1-negative cell lines CC4A and CH72T3. Molecular weights of marker proteins are indicated in the left margin, arrows indicate adenylyl cyclase isoforms showing differential expression. E. Western blot analysis using AC isoform specific antibodies against ACIII, ACV/VI, ACVII and ACIX in VILIP-1-positive cell lines CC4B and CH72 compared to more aggressive VILIP-1-negative cell lines CC4A and CH72T3. Protein markers are indicated in the left margins, arrows indicate adenylyl cyclase isoforms showing differential expression and β-actin bands are shown as loading control.