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. Author manuscript; available in PMC: 2011 Feb 16.
Published in final edited form as: J Biol Chem. 2006 Aug 30;281(45):34601–34609. doi: 10.1074/jbc.M601530200

FIGURE 8. CD44 internalization is dependent on receptor palmitoylation.

FIGURE 8

The two channel fluorescence overlay images of cells (A and B) represent another illustration of the loss of CD44 expression in COS-7 transfectants of CD44wt at time zero (A) as compared with 3 h following pre-treatment with cycloheximide (B). As in Fig. 7, the red fluorescence represents immunostaining of the cells with anti-CD44 monoclonal antibody, BU-52, followed by anti-mouse Cy3-conjugated secondary antibody. C depicts CD44 Western blotting of cell lysates prepared from COS-7 transfectants at time zero (lanes 1, 3, and 5) or after 6 h of treatment with cycloheximide (lanes 2, 4, and 6). Lysates of wild-type CD44 (CD44wt; lanes 1 and 2), CD44-C286A (lanes 3 and 4), or CD44-C286,295A (lanes 5 and 6) were examined. D represents a CD44 Western blot of another experiment that depicts transfectants of CD44H (lanes 1–3) or CD44-C286,295A (lanes 4 and 5) at time zero (lanes 1 and 4), treated with cycloheximide for 3 h (lanes 2 and 5) or treated with cycloheximide and chloroquine for 3 h (lane 3). Changes in band intensity were quantified by digital scanning of x-ray films, and the resultant data are expressed as the average ± S.D. (n = 3) change in pixel density relative to control CD44 wild-type expression.