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- W3194144433 startingPage "1982" @default.
- W3194144433 abstract "The electron transport chain promotes aspartate synthesis, which is required for cancer cell proliferation. However, it is unclear whether aspartate is limiting in normal stem cells. We found that mouse hematopoietic stem cells (HSCs) depend entirely on cell-autonomous aspartate synthesis, which increases upon HSC activation. Overexpression of the glutamate/aspartate transporter, Glast, or deletion of glutamic-oxaloacetic transaminase 1 (Got1) each increased aspartate levels in HSCs/progenitor cells and increased the function of HSCs but not colony-forming progenitors. Conversely, deletion of Got2 reduced aspartate levels and the function of HSCs but not colony-forming progenitors. Deletion of Got1 and Got2 eliminated HSCs. Isotope tracing showed aspartate was used to synthesize asparagine and purines. Both contributed to increased HSC function as deletion of asparagine synthetase or treatment with 6-mercaptopurine attenuated the increased function of GLAST-overexpressing HSCs. HSC function is thus limited by aspartate, purine, and asparagine availability during hematopoietic regeneration." @default.
- W3194144433 created "2021-08-30" @default.
- W3194144433 creator A5020716844 @default.
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- W3194144433 date "2021-11-01" @default.
- W3194144433 modified "2023-10-15" @default.
- W3194144433 title "Aspartate availability limits hematopoietic stem cell function during hematopoietic regeneration" @default.
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- W3194144433 doi "https://doi.org/10.1016/j.stem.2021.07.011" @default.
- W3194144433 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8571029" @default.
- W3194144433 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34450065" @default.
- W3194144433 hasPublicationYear "2021" @default.
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