Abstract
Transcription co-regulator Cited2 is essential for mouse development. Recent work has shown that Cited2 plays important roles in normal hematopoiesis in fetal liver and adult bone marrow. This review focuses on the function of Cited2 in the maintenance of hematopoietic stem cells (HSCs) and its potential role in the metabolic regulation of HSCs. Fetal liver cells from Cited2 null embryos give rise to reduced numbers of hematopoietic colonies and display significantly impaired hematopoietic reconstitution capacity. In adult mice, conditional deletion of Cited2 markedly reduces the number of HSCs and compromises hematopoietic reconstitution in mice receiving a transplant of Cited2 deficient bone marrow cells. Additional deletion of Ink4a/Arf or p53 in a Cited2-deficient background restores HSC functionality. Meanwhile, Cited2 deficient HSCs display loss of quiescence, which can be partially rescued by additional deletion of hypoxia inducible factor-1α. Cited2 is an essential regulator in fetal liver and adult hematopoiesis. Further studies into the function of Cited2 and the underlying mechanism in the metabolic regulation of HSCs will provide a better understanding of the connection between energy metabolism and HSC quiescence and self-renewal. Investigations of the pathologic role of Cited2 in leukemogenesis may yield useful information in developing effective therapeutic strategies.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
