Figure 1.
ASF1B is upregulated in AML progenitors upon IL-1β stimulation. (A) RNA-seq analysis was performed using purified CD34+ cells derived from the bone marrow of patients with AML (n = 3) and healthy donors (n = 3). Cells were cultured with 10 ng/mL IL-1β or vehicle control for 2 days. The heat map indicates log2 counts per million (CPM) of differentially expressed genes in vehicle- or IL-1β–treated healthy and AML CD34+ bone marrow cells. (B) STRING-DB network analysis of genes upregulated in IL-1β–treated AML cells vs IL-1β–treated healthy cells. (C) TLDA analysis was performed on AML (n = 4) and healthy CD34+ (n = 4) bone marrow cells treated with or without 10 ng/mL IL-1β for 2 days. The expression of listed genes is shown as a fold difference upon IL-1β stimulation compared with respective vehicle controls in AML and healthy CD34+ bone marrow cells. (D) Schematic representation of the TLK-ASF1 pathway. (E) Immunoblot of TLKs and ASF1s protein expression in CD34+ bone marrow cells from healthy donors (n = 5) and patient-derived AML samples (n = 14) with indicated mutations. (F) Densitometry analysis of the immunoblot is shown and expressed as means ± standard error of the mean (SEM). Student t test was used for statistical analysis. ∗P < .05.

ASF1B is upregulated in AML progenitors upon IL-1β stimulation. (A) RNA-seq analysis was performed using purified CD34+ cells derived from the bone marrow of patients with AML (n = 3) and healthy donors (n = 3). Cells were cultured with 10 ng/mL IL-1β or vehicle control for 2 days. The heat map indicates log2 counts per million (CPM) of differentially expressed genes in vehicle- or IL-1β–treated healthy and AML CD34+ bone marrow cells. (B) STRING-DB network analysis of genes upregulated in IL-1β–treated AML cells vs IL-1β–treated healthy cells. (C) TLDA analysis was performed on AML (n = 4) and healthy CD34+ (n = 4) bone marrow cells treated with or without 10 ng/mL IL-1β for 2 days. The expression of listed genes is shown as a fold difference upon IL-1β stimulation compared with respective vehicle controls in AML and healthy CD34+ bone marrow cells. (D) Schematic representation of the TLK-ASF1 pathway. (E) Immunoblot of TLKs and ASF1s protein expression in CD34+ bone marrow cells from healthy donors (n = 5) and patient-derived AML samples (n = 14) with indicated mutations. (F) Densitometry analysis of the immunoblot is shown and expressed as means ± standard error of the mean (SEM). Student t test was used for statistical analysis. ∗P < .05.

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