Oncogenic roles of PRL-3 in FLT3-ITD induced acute myeloid leukaemia
Article first published online: 8 AUG 2013
Copyright © 2013 EMBO Molecular Medicine
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
EMBO Molecular Medicine
Volume 5, Issue 9, pages 1351–1366, September 2013
How to Cite
Park, J. E., Yuen, H. F., Zhou, J. B., Al-aidaroos, A. Q. O., Guo, K., Valk, P. J., Zhang, S. D., Chng, W. J., Hong, C. W., Mills, K. and Zeng, Q. (2013), Oncogenic roles of PRL-3 in FLT3-ITD induced acute myeloid leukaemia. EMBO Mol Med, 5: 1351–1366. doi: 10.1002/emmm.201202183
- Issue published online: 3 SEP 2013
- Article first published online: 8 AUG 2013
- Manuscript Accepted: 20 JUN 2013
- Manuscript Revised: 18 JUN 2013
- Manuscript Received: 19 OCT 2012
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Figure S1. Quantitative real-time PCR analysis for AML patients' bone marrow samples: high PRL-3 mRNA expression was associated with AML patients with FLT3-ITD mutation.
Figure S2. STAT5A and STAT5B protein expression levels with different reporter vectors.
Figure S3. AP-SEAP activity assay in DLD-1 and HCT116 cells: PRL-3 overexpression activates AP-1 activity.
Figure S4. Annexin-V and 7-AAD staining with MOLM-14 and MV4-11 cells: Depletion of PRL-3 shows no substantial increment in apoptotic population in two cytokine independent cell lines, MOLM-14 and MV4-11.
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