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 Blood, 1 October 2007, Vol. 110, No. 7, pp. 2704-2707.
Prepublished online as a Blood First Edition Paper on July 6, 2007; DOI 10.1182/blood-2006-12-064154.

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Submitted December 19, 2006
Accepted June 27, 2007

Cul4A is required for hematopoietic stem cell engraftment and self-renewal

Binghui Li, Nan Jia, David L. Waning, Feng-Chun Yang, Laura S. Haneline, and Kristin T. Chun*

Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, United States
Department of Microbiology & Immunology, Indiana University School of Medicine, Indianapolis, IN, United States
Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, United States

* Corresponding author; email: kchun{at}iupui.edu.

Several hematopoietic stem cell (HSC) regulators are controlled by ubiquitin-mediated proteolysis, so the ubiquitin pathway might modulate HSC function. However, this hypothesis has not been formally tested. Cul4A encodes a core subunit of one ubiquitin ligase. Whereas Cul4A-deficient embryos die in utero, Cul4A haploinsufficient mice are viable but exhibit abnormal hematopoiesis (fewer erythroid and primitive myeloid progenitors). Given these data, we examined whether Cul4A +/- HSCs might also be impaired. Using bone marrow transplantation assays, we determined that Cul4A +/- HSCs exhibit defects in engraftment and self-renewal capacity. These studies are the first to demonstrate that ubiquitin-mediated protein degradation is important for HSC function. Further, they indicate that a Cul4A ubiquitin ligase targets for degradation one or multiple HSC regulators.


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D. L. Waning, B. Li, N. Jia, Y. Naaldijk, W. S. Goebel, H. HogenEsch, and K. T. Chun
Cul4A is required for hematopoietic cell viability and its deficiency leads to apoptosis
Blood, July 15, 2008; 112(2): 320 - 329.
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