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BUBR1 deficiency results in abnormal megakaryopoiesis
Open accessAbstract
The physiologic function of BUBR1, a key component of the spindle checkpoint, was examined by generating BUBR1-mutant mice. BUBR1(-/-) embryos failed to survive beyond day 8.5 in utero as a result of extensive apoptosis. Whereas BUBR1(+/-) blastocysts grew relatively normally in vitro, BUBR1(-/-) blastocysts exhibited impaired proliferation and atrophied. Adult BUBR1(+/-) mice manifested splenomegaly and abnormal megakaryopoiesis. BUBR1 haploinsufficiency resulted in an increase in the number of splenic megakaryocytes, which was correlated with an increase in megakaryocytic, but a decrease in erythroid, progenitors in bone marrow cells. RNA interference-mediated down-regulation of BUBR1 also caused an increase in polyploidy formation in murine embryonic fibroblast cells and enhanced megakaryopoiesis in bone marrow progenitor cells. However, enhanced megakaryopoiesis in BUBR1(+/-) mice was not correlated with a significant increase in platelets in peripheral blood, which was at least partly due to a defect in the formation of proplatelet-producing megakaryocytes. Together, these results indicate that BUBR1 is essential for early embryonic development and normal hematopoiesis.
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Metadata
- Authors
- Wang, Q.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2003-10-23
- Volume
- 103
- Issue
- 4
- Pages
- 1278-1285
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2123154779
- Cited by
- 183
- References
- 0
- FWCI
- 5.20
- Type
- journal article
- Language
- en
- Open access
- bronze
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