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. 2021 Feb 12;22(4):1825. doi: 10.3390/ijms22041825

Figure 4.

Figure 4

Effect of Bam32 deficiency on CXCL2-induced Rac1, Rac2, and Rap1 activation in neutrophils. (A) Levels of Rac1-GTP in bone marrow-derived neutrophils from WT and Bam32−/− mice with saline (0 s) and after the stimulation of neutrophils with CXCL2 (0.1 µM) for 30, 60, and 120 s. (B,C) Representative original Western blots and the levels of Rac2-GTP (B) and Rap1-GTP (C) determined in bone marrow-derived neutrophils from WT and Bam32−/− mice at 2 min after the stimulation of neutrophils with CXCL2 (0.1 µM). (D) Representative original Western blots and the levels of Rap1-GTP and total Rap1 determined in bone marrow-derived neutrophils from WT and Bam32−/− mice at 2 min after the stimulation of neutrophils with CXCL2 (0.1 µM) and with pre-treatment with DMSO (vehicle) or Rac1 inhibitor NSC23766 (50 µM) for 30 min and throughout the 2-min CXCL2 stimulation. (A−D): mean ± SEM of 3 samples per group. Each sample was individually collected and pooled from two mice of the same strain. The Rac1 G-LISA assay was performed twice in the 96-well plate. * and ** indicate significant differences (p < 0.05 and p < 0.01, respectively) from WT mice (C,D) or from WT mice without NSC23766.