Endogenous DNA Damage Leads to p53-Independent Deficits in Replicative Fitness in Fetal Murine Fancd2−/− Hematopoietic Stem and Progenitor Cells
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- 作者：Young me Yoon1 ; 2 ; 3 ; Kelsie J. Storm1 ; 2 ; 3 ; 5 ; Ashley N. Kamimae-Lanning1 ; 2 ; 3 ; 6 ; Natalya A. Goloviznina1 ; 2 ; 3 ; 7 ; Peter Kurre1 ; 2 ; 3 ; 4 ; kurrepe@ohsu.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：Fanconi anemia ; hematopoiesis ; stem cells ; development ; bone marrow failure
- 刊名：Stem Cell Reports
- 出版年：2016
- 出版时间：8 November 2016
- 年：2016
- 卷：7
- 期：5
- 页码：840-853
- 全文大小：2559 K
文摘
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Fancd2−/− fetal HSPCs show spontaneous deficits on replicative stress in development
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Fancd2−/− FL HSPCs show activated DNA-damage responses and strand-break accumulation
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Fancd2−/− FL deficits occur without apoptosis and independent of p53 activation
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MAPK (p38) inhibition rescues Fancd2−/− progenitor defects in vitro and in vivo