Fig. 1: Identification of a transcriptional signature of hyperactivated CXCR4 signaling.
From: CXCR4 hyperactivation cooperates with TCL1 in CLL development and aggressiveness
a Illustration of the CXCR4C1013G truncating mutation and outline of experimental setup for immunoblotting and RNA sequencing of splenic and bone marrow B cells. b Representative image of immunoblotting for AKT, pAKT (Ser473), ERK, pERK (Thr202/Tyr204), and Actin of CD19+ B cells treated with/without 50 nM CXCL12 and/or 10 µM CXCR4 inhibitor AMD3100 (AMD) (WT, n = 3; CXCR4C1013G, n = 3). c Relative pAKT to AKT and pERK to ERK protein expression by immunoblotting of WT and CXCR4C1013G CD19+ B cells treated with/without 50 nM CXCL12 and/or 10 µM CXCR4 inhibitor AMD3100 (WT, n = 3; CXCR4C1013G, n = 3). d Volcano plot showing differentially expressed genes (DEG) of CXCR4C1013G vs. WT CD19+ B cells (WT, n = 5; CXCR4C1013G, n = 5). e Gene set enrichment analysis (GSEA) of CXCR4C1013G vs. WT CD19+ B cells showing normalized enrichment scores (NES) and false discovery rates (FDR) for curated gene sets listed in MsigDB [63, 64] of CXCR4C1013G compared to WT CD19+ B cells. Statistical analyses were performed with one-way ANOVA with Tukey correction for multiple comparisons, *P < 0.05, **P < 0.01, ***P < 0.001. Error bars indicate standard deviation (SD).
