Figure 3
Syk was required for the translocation of mAbp1 to the site of particle binding. Confocal microscopy images of (A) murine Syk+/+ and Syk−/− PMNs and (B-C) piceatannol-treated (PIC) and untreated (control) dHL-60 cells phagocytosing serum-opsonized Alexa 594–conjugated E coli (red). (A) Translocation of mAbp1 (green) to the site of particle binding was severely compromised in Syk−/− PMNs (arrowheads) compared with Syk+/+ PMNs in which mAbp1 was distinctly enriched at the site of particle binding (arrows). (B) On inhibition of Syk with 30μM piceatannol (PIC), the translocation of mAbp1 to the site of particle binding was impaired (arrowheads) compared with DMSO-treated dHL-60 control cells (arrows). (C) Translocation of CD18 (green) to the site of particle binding was not affected by the inhibition of Syk (↑,) in dHL-60 cells. Images are representative for 3 independent experiments. Bar = 10 μm.

Syk was required for the translocation of mAbp1 to the site of particle binding. Confocal microscopy images of (A) murine Syk+/+ and Syk−/− PMNs and (B-C) piceatannol-treated (PIC) and untreated (control) dHL-60 cells phagocytosing serum-opsonized Alexa 594–conjugated E coli (red). (A) Translocation of mAbp1 (green) to the site of particle binding was severely compromised in Syk−/− PMNs (arrowheads) compared with Syk+/+ PMNs in which mAbp1 was distinctly enriched at the site of particle binding (arrows). (B) On inhibition of Syk with 30μM piceatannol (PIC), the translocation of mAbp1 to the site of particle binding was impaired (arrowheads) compared with DMSO-treated dHL-60 control cells (arrows). (C) Translocation of CD18 (green) to the site of particle binding was not affected by the inhibition of Syk (↑,) in dHL-60 cells. Images are representative for 3 independent experiments. Bar = 10 μm.

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