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. Author manuscript; available in PMC: 2015 Jun 1.
Published in final edited form as: J Immunol. 2014 Apr 28;192(11):5305–5313. doi: 10.4049/jimmunol.1302983

Figure 9. FPR1 mediated PKC activation, and role of PKCβ in the cross-phosphorylation of CCR1.

Figure 9

HR1R2F cells were treated with 0.5 μM fMLF for the designated times (A) or doses of fMLF for 20 min (B & C), followed by western blot analysis of phosphor-PKC using antibodies for phosphorylated PKCβ1 (Thr 642) (A), anti-phospho-PKCβII (Thr638/641) (B), and anti-phospho-PKC θ (Thr538) (C) antibodies. GAPDH was also probed as loading controls. (D) Cells were also pretreated with 1 μM PKCβ pseudosubstrate inhibitor (PPβi) 20 min, followed by treatment with vehicle or 0.5 μM fMLF or 10 nM CCL3 for 20 min. The assessment of phosphorylation of CCR1 was then carried out as described in the Materials and Methods. CCR1 and GAPDH were also analyzed to control for loading. The normalized absorbance of each of the phosphorylated bands is presented below the GAPDH panel (panels A & B). The densitometry results for 3 replicate experiments are shown for panel D).