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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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Brief Report

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

Binghui Li1,2, Nan Jia1,2, David L. Waning1,2, Feng-Chun Yang1,2, Laura S. Haneline1,2,4, and Kristin T. Chun1,2,3

1 Herman B Wells Center for Pediatric Research, Departments of2 Pediatrics, 3 Biochemistry and Molecular Biology, and 4 Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN

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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