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letter
. 2017 Dec 22;7(12):661. doi: 10.1038/s41408-017-0031-x

Fig. 1. ANP32A dysregulation contributes to AMKL.

Fig. 1

a The expression of ANP32A mRNA in HSC CD133+CD34dim, MEP (megakaryocyte-erythrocyte progenitor), CFU-Mk (colony-forming unit-megakaryocyte), and Mk (megakaryocytes) were analyzed and presented as log 2 expression. Expression data were obtained from online Bloodspot database (http://servers.binf.ku.dk/bloodspot/?gene=C5orf4&dataset=DMAP). b Quantitative RT-PCR analysis of ANP32A in MNCs from healthy donors (Normal, N=5) and two cases of AMKL patients (AMKL#1 and #2). The expression of ANP32A was normalized to GAPDH and presented as relative mRNA level. ***p < 0.001; NS: not significant. c Immunoblotting to detect ANP32A expression and flow cytometry to measure the expression of CD41 and CD42. Histograms were representative results of three independent experiments (duplicates) with similar results. d Scramble or Anp32a-knockdown (shAnp32a#1) 6133/MPL W515L cells were seeded in soft agar to measure the CFU. *p < 0.05. e Scramble or ANP32A-knockdown 6133/MPL W515L cells (shANP32A#1) were transplanted into semi-lethally irradiated mice through retro-orbital injection. The mice survival was observed up to 7 weeks