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Isotope tracing, mathematical modeling, and single-cell ATP analysis reveal changes in blood cell metabolism under various conditions, showing stressed hematopoietic stem cells support hematopoiesis through glycolytic ATP production via PFKFB3.

Mass spectrometry exposes a post-transcriptionally regulated reduction in protein diversity in hematopoietic stem cells, including a lack of detectable Dnmt3a protein levels despite mRNA levels comparable to progenitors.

In vivo modulation of the prostaglandin, interferon, or granulocyte colony-stimulating factor pathway induces rapid and specific transcriptional changes in hematopoietic stem cells with significant heterogeneity in the cellular response.

Application of a polyvinyl alcohol-based culture system reveals extensive differentiation but simultaneous robust murine hematopoietic stem cell (HSC) expansion, which are characterized by phenotypic, functional, and molecular properties shared with freshly isolated bone marrow HSCs.

A gene-centric functional screen uncovers biological mechanisms underlying genome-wide association study signals for human red blood cell traits.

Normal hematopoietic stem and progenitor cells slow the regeneration of their niche after injury to minimize leakage from the niche vasculature.

DDB1, a component of the ubiquitin proteasome system, plays a role in both hematopoietic and embryonic stem cell self-renewal and differentiation.

Two niches contribute to the control of Drosophila blood cell homeostasis through their differential regulation of hematopoietic progenitors.

Chronic and excessive inflammation can lead to exhaustion of the supply of hematopoietic stem cells and to myeloid malignancies in mice, mimicking important aspects of the myelodysplastic syndrome found in humans.

Identification of Hematopoietic stem cells (HSCs) in the genetically amenable organism Drosophila melanogaster paves the path to address HSC biology, both in normal and pathophysiological conditions.