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. 2013 Oct 8;123(11):4627–4640. doi: 10.1172/JCI70739

Figure 3. Downregulation of Clec5a caused by ASXL1-MT played a pivotal role in differentiation block.

Figure 3

(A and B) 32Dcl3 cells transduced with pMYs-IP/pMYs-IB, pMYs-IP/ pMYs-ASXL1-MT2-IB, pMYs-Clec5a-IP/pMYs-ASXL1-MT2-IB, and pMYs-Clec5a-K16A-IP/pMYs-ASXL1-MT2-IB were cultured in the presence of 50 ng/ml G-CSF for 6 days. The proportions of mature or immature cells (A) and cytospin preparations of these cells (B) are shown. Images were obtained with a BX51 microscope and an Olympus DP12 camera with a UplanFl objective lens. Original magnification, ×40; scale bars: 20 μm. Data are representative of 3 independent experiments. (C) Relative expression levels of CLEC5A were examined by qRT- PCR in whole BM cells derived from normal controls and from patients with ASXL1-mutated MDS and ASXL1-WT MDS. The values were normalized by GAPDH mRNA levels. All data with error bars are presented as mean ± SEM of 2 independent experiments. P values were calculated using the 2-tailed Student’s t test or the Cochran-Cox test.