Fig 1: Competitive attenuation of murine CSF2‑induced JAK2/STAT5 activation, ROS production, and phagocytosis by KCR. (A, C) Western blot analysis of competitive attenuation of murine CSF2‐induced p‐JAK2 and p‐STAT5 in macrophages by KCR. (B, D) Densitometric quantification of p‐JAK2 and p‐STAT5 levels from (A) and (C), respectively. (E) Competitive attenuation of CSF2‐induced mean FITC intensity in contour plot of flow cytometry by KCR. (F) Competitive attenuation of CSF2‐induced phagocytosis in macrophages by KCR. (G) Competitive attenuation of CSF2‐induced ROS production in macrophages by KCR. ∗ p < 0.05 and ∗∗∗∗ p < 0.0001.
Fig 2: Activation of the JAK2/STAT5 pathway by KCR in macrophages. (A, C) Western blot analysis of phosphorylated JAK2 (p‐JAK2) and STAT5 (p‐STAT5) in RAW264.7 mouse macrophages stimulated with murine CSF2. (B, D) Densitometric quantification of p‐JAK2 and p‐STAT5 levels from (A) and (C), respectively. (E, G) Western blot analysis of p‐JAK2 and p‐STAT5 in RAW264.7 macrophages stimulated with KCR. (F, H) Densitometric quantification of p‐JAK2 and p‐STAT5 levels from (E) and (G), respectively. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗∗ p < 0.0001.
Fig 3: Promotion of phagocytosis mediated by complement/Fc/scavenger receptor by KCR. (A) Enhancement of mean FITC intensity in contour plot of flow cytometry by KCR. (B) Phagocytosis in murine macrophages stimulated with CSF2. (C–G) Transcription levels of complement (CR3), Fc (CD16 and CD64), and scavenger receptor (MSR1 and MARCO) in murine macrophages following KCR stimulation. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.
Fig 4: Enhancement of the ROS production based on NADPH oxidase catalysis by KCR. (A) ROS production in murine macrophages treated with CSF2. (B) ROS production in murine macrophages treated with KCR. (C–F) Transcription levels of the NADPH oxidase subunits gene CYBB, CYBA, NCF1, and NCF2 in murine macrophages following KCR stimulation. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.
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