Blocked O-GlcNAc cycling disrupts mouse hematopoeitic stem cell maintenance and early T cell development
Author:
Funder
U.S. Department of Health & Human Services | NIH | National Cancer Institute
Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/s41598-019-48991-8.pdf
Reference68 articles.
1. Simsek, T. et al. The distinct metabolic profile of hematopoietic stem cells reflects their location in a hypoxic niche. Cell stem cell 7, 380–390, https://doi.org/10.1016/j.stem.2010.07.011 (2010).
2. Takubo, K. et al. Regulation of glycolysis by Pdk functions as a metabolic checkpoint for cell cycle quiescence in hematopoietic stem cells. Cell stem cell 12, 49–61, https://doi.org/10.1016/j.stem.2012.10.011 (2013).
3. Ma, J. & Hart, G. W. O-GlcNAc profiling: from proteins to proteomes. Clin Proteomics 11, 8, https://doi.org/10.1186/1559-0275-11-8 (2014).
4. Hanover, J. A., Chen, W. & Bond, M. R. O-GlcNAc in cancer: An Oncometabolism-fueled vicious cycle. Journal of bioenergetics and biomembranes, https://doi.org/10.1007/s10863-018-9751-2 (2018).
5. Shafi, R. et al. The O-GlcNAc transferase gene resides on the X chromosome and is essential for embryonic stem cell viability and mouse ontogeny. Proceedings of the National Academy of Sciences of the United States of America 97, 5735–5739, https://doi.org/10.1073/pnas.100471497 (2000).
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