Embryonic Stem Cells/induced Pluripotent Stem Cells
Article first published online: 24 APR 2013
Copyright © 2013 AlphaMed Press
Volume 31, Issue 5, pages 1022–1029, May 2013
How to Cite
Yung, S. K., Tilgner, K., Ledran, M. H., Habibollah, S., Neganova, I., Singhapol, C., Saretzki, G., Stojkovic, M., Armstrong, L., Przyborski, S. and Lako, M. (2013), Brief Report: Human Pluripotent Stem Cell Models of Fanconi Anemia Deficiency Reveal an Important Role for Fanconi Anemia Proteins in Cellular Reprogramming and Survival of Hematopoietic Progenitors. STEM CELLS, 31: 1022–1029. doi: 10.1002/stem.1308
Author contributions: S.Y., K.T., and M.L.: performed experiments, data analysis, and final approval of manuscript; S.H., I.N., C.S., and G.S.: performed some of the experiments and final approval of manuscript; M.S.: conception and design, fund raising, and final approval of manuscript; L.A.: conception and design, manuscript writing, fund raising, and final approval of manuscript; S.P.: performed some of the experiments, collection and analysis of the data, contributed to manuscript writing, and final approval of manuscript; M.L.: conception and design, performed experiments, data analysis, manuscript writing, fund raising, and final approval of manuscript. S.K.Y. and K.T. contributed equally to this article.
Disclosure of potential conflicts of interest is found at the end of this article.
First published online in STEM CELLSEXPRESS December 27, 2012.
- Issue published online: 24 APR 2013
- Article first published online: 24 APR 2013
- Accepted manuscript online: 27 DEC 2012 01:44AM EST
- Manuscript Accepted: 1 DEC 2012
- Manuscript Received: 2 AUG 2012
- Leukemia and Lymphoma Research. Grant Number: 10050
- Fanconi Anemia Research Fund U.S.
- Fanconi Hope U.K.
- Regenerative Medicine through the collaboration agreement from the Conselleria de Sanidad (Generalitat Valenciana)
- Instituto de Salud Carlos III (Ministry of Science and Innovation), Spain
Additional Supporting Information may be found in the online version of this article.
|sc-12-0715_sm_SupplFigure1.pdf||239K||Suppl. Figure 1. Transduction with a control GFP lentiviral construct shows no significant differences in transduction efficiency between control (NHDF = neonatal human dermal fibroblasts) and FANCC fibroblasts.|
|sc-12-0715_sm_SupplFigure2.pdf||220K||Suppl. Figure 2. DNA fingerprinting of FANCC hiPSC (bottom panel) showing identical DNA genetic profiles with the fibroblast (upper panels) they were derived from respectively.|
|sc-12-0715_sm_SupplFigure3.pdf||214K||Suppl. Figure 3. FA functionality pathway assays measuring the number of FANCD2 foci in response to mitomycin C treatment. Representative images showing activation of FA pathway and red FANCD2 foci accumulation in control hESC and hiPSC. In contrary, no activation of FA pathway was observed in the FANCC hESC/hiPSC clones.|
|sc-12-0715_sm_SupplTable1.pdf||423K||Supplementary Table 1. Summary of hiPSC lines derived from FANC deficient patients together with reprogramming efficiency.|
Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.