ArticleJCI insight2019
PI3 kinase alpha and delta promote hematopoietic stem cell activation.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Lymphoproliferation in Inborn Errors of Immunity: Mechanisms, Manifestations and Clinical Management, with a Focus on ALPID.ImmunoTargets and therapy · 2026Review
- P-selectin overexpression impairs hematopoietic stem cell homeostasis via inflammatory receptor-mediated proliferation and differentiation.Cell death & disease · 2025Article
- Linking mitochondria, fatty acids, and hematopoietic stem cell expansion during infection: implications for aging and metabolic diseases.Stem cells (Dayton, Ohio) · 2025Review
- Deciphering and targeting oncogenic pathways through integrated approaches and amino acid metabolism in hematologic malignancies.Discover oncology · 2025Review
- Network pharmacology and experimental verification of the potential mechanism of Er-Xian decoction in aplastic anemia.Scientific reports · 2023Article
- Human T-Cell Leukemia Virus Type 1 Oncogenesis between Active Expression and Latency: A Possible Source for the Development of Therapeutic Targets.International journal of molecular sciences · 2023Review
- Regulation of adult stem cell quiescence and its functions in the maintenance of tissue integrity.Nature reviews. Molecular cell biology · 2023Review
- Crizotinib Has Preclinical Efficacy in Philadelphia-Negative Myeloproliferative Neoplasms.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- PI3-kinase deletion promotes myelodysplasia by dysregulating autophagy in hematopoietic stem cells.Science advances · 2023Article
- PU.1 is required to restrain myelopoiesis during chronic inflammatory stress.Frontiers in cell and developmental biology · 2023Article
- Regulation of hematopoietic stem cells differentiation, self-renewal, and quiescence through the mTOR signaling pathway.Frontiers in cell and developmental biology · 2023Review
- Physioxia-induced downregulation of Tet2 in hematopoietic stem cells contributes to enhanced self-renewal.Blood · 2022Article
- Class I PI3K regulatory subunits control differentiation of dendritic cell subsets and regulate Flt3L mediated signal transduction.Scientific reports · 2022Article
- Phosphoinositide 3-Kinases as Potential Targets for Thrombosis Prevention.International journal of molecular sciences · 2022Review
- Molecular regulation of hematopoietic stem cell quiescence.Cellular and molecular life sciences : CMLS · 2022Review
- Host T Cell Dedifferentiation Effects Drive HIV-1 Latency Stability.Journal of virology · 2022Article
- Membrane-bound SCF and VCAM-1 synergistically regulate the morphology of hematopoietic stem cells.The Journal of cell biology · 2021Article
- PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress.The Journal of experimental medicine · 2021Article
- Regulation of stress-induced hematopoiesis.Current opinion in hematology · 2020Review
- The metalloproteinase Papp-aa controls epithelial cell quiescence-proliferation transition.eLife · 2020Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
Many cytokines and chemokines that are important for hematopoiesis activate the PI3K signaling pathway. Because this pathway is frequently mutated and activated in cancer, PI3K inhibitors have been developed for the treatment of several malignancies, and are now being tested in the clinic in combination with chemotherapy. However, the role of PI3K in adult hematopoietic stem cells (HSCs), particularly during hematopoietic stress, is still unclear. We previously showed that the individual PI3K catalytic isoforms P110α or P110β have dispensable roles in HSC function, suggesting redundancy between PI3K isoforms in HSCs. We now demonstrate that simultaneous deletion of P110α and P110δ in double knockout (DKO) HSCs uncovers their redundant requirement in HSC cycling after 5-fluorouracil (5-FU) chemotherapy administration. In contrast, DKO HSCs are still able to exit quiescence in response to other stress stimuli, such as LPS. We found that DKO HSCs and progenitors have impaired sensing of inflammatory signals ex vivo, and that levels of IL1-β and MIG are higher in the bone marrow after LPS than after 5-FU administration. Furthermore, exogenous in vivo administration of IL1-β can induce cell cycle entry of DKO HSCs. Our findings have important clinical implications for the use of PI3K inhibitors in combination with chemotherapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.