Fig. 8: KRAS-mutant human leukemia cells exhibit increased NLRP3 inflammasome activation.
From: Oncogenic KrasG12D causes myeloproliferation via NLRP3 inflammasome activation
a Western blot shows the amount of caspase-1 (p20 subunit) in PBMCs isolated from patients with a KRAS mutation (Krasmut) or without a KRAS mutation (non-Krasmut). The blot is representative for four independent experiments. b The ratio of caspase-1 (p20 subunit)/β-actin in Krasmut (n = 8) or non-Krasmut (n = 8) patients’ PBMCs normalized to non-Krasmut. c The histogram shows mean fluorescence intensity (MFI) for IL-1β in CD11b+ cells of Krasmut JMML or non- Krasmut AML patients. One representative experiment from four experiments with is shown. d–e The graphs display the fold change of IL-1β expression as measured by flow cytometry in (d) Krasmut JMML (n = 9) and (e) Krasmut AML (n = 11), compared to non-Krasmut AML patients’ PBMCs (n = 22), normalized to non-Krasmut. (f) The histogram shows mean fluorescence intensity (MFI) for IL-1β in CD11b+ cells of Krasmut or non-Krasmut CMML patients’ cells. One representative experiment from four experiments is shown. (g) The graph displays MFI fold change of IL-1β expression as measured by flow cytometry in Krasmut (n = 5) and non-Krasmut (n = 13) CMML patients’ PBMCs, normalized to non-Krasmut. h Western blot shows the amount of caspase-1 (p20 subunit) in PBMCs isolated from CMML patients with a KRAS mutation (Krasmut) or without a KRAS mutation (non-Krasmut). i The ratio of caspase-1 (p20 subunit)/Vinculin in Krasmut (n = 4) or non-Krasmut (n = 4) CMML patients’ PBMCs normalized to non-Krasmut.
