ArticleBlood2015
IP3 3-kinase B controls hematopoietic stem cell homeostasis and prevents lethal hematopoietic failure in mice.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- ITPKB is a conserved regulator of natural killer cell desensitization/education that constrains antitumor immunity.bioRxiv : the preprint server for biology · 2026Article
- A sustained-release depot formulation of β-nicotinamide mononucleotide for alleviating chemotherapy-induced myelosuppression.Materials today. Bio · 2026Article
- Physiological roles of phosphoinositides and inositol phosphates: Implications for metabolic dysfunction-associated steatotic liver disease.Clinical science (London, England : 1979) · 2025Review
- Origin, evolution, and diversification of inositol 1,4,5-trisphosphate 3-kinases in plants and animals.BMC genomics · 2024Article
- Evidence that inositol 1,4,5-trisphosphate 3-kinase and inositol 1,3,4,5-tetrakisphosphate are negative regulators of platelet function.Research and practice in thrombosis and haemostasis · 2024Article
- Molecular mechanisms of cellular metabolic homeostasis in stem cells.International journal of oral science · 2023Review
- Regulation of adult stem cell quiescence and its functions in the maintenance of tissue integrity.Nature reviews. Molecular cell biology · 2023Review
- Regulation of hematopoietic stem cells differentiation, self-renewal, and quiescence through the mTOR signaling pathway.Frontiers in cell and developmental biology · 2023Review
- Identification of a prognostic metabolic gene signature in diffuse large B-cell lymphoma.Journal of cellular and molecular medicine · 2021Article
- Adaptive responses toProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Regulation of Hematopoietic Stem Cell Fate and Malignancy.International journal of molecular sciences · 2020Review
- Isoform-specific involvement of Brpf1 in expansion of adult hematopoietic stem and progenitor cells.Journal of molecular cell biology · 2020Article
- Severe combined immunodeficiency caused by inositol-trisphosphate 3-kinase B (ITPKB) deficiency.The Journal of allergy and clinical immunology · 2020Article
- Article
- Inositol-triphosphate 3-kinase B confers cisplatin resistance by regulating NOX4-dependent redox balance.The Journal of clinical investigation · 2019Article
- Article
- mTOR signaling in stem and progenitor cells.Development (Cambridge, England) · 2018Review
- Regulation of Hematopoietic Cell Development and Function Through Phosphoinositides.Frontiers in immunology · 2018Review
- Inositol-1,4,5-trisphosphate 3-kinase-A (ITPKA) is frequently over-expressed and functions as an oncogene in several tumor types.Biochemical pharmacology · 2017Review
- LECT2 drives haematopoietic stem cell expansion and mobilization via regulating the macrophages and osteolineage cells.Nature communications · 2016Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Tight regulation of hematopoietic stem cell (HSC) homeostasis ensures lifelong hematopoiesis and prevents blood cancers. The mechanisms balancing HSC quiescence with expansion and differentiation into hematopoietic progenitors are incompletely understood. Here, we identify Inositol-trisphosphate 3-kinase B (Itpkb) as an essential regulator of HSC homeostasis. Young Itpkb(-/-) mice accumulated phenotypic HSC, which were less quiescent and proliferated more than wild-type (WT) controls. Itpkb(-/-) HSC downregulated quiescence and stemness associated, but upregulated activation, oxidative metabolism, protein synthesis, and lineage associated messenger RNAs. Although they had normal-to-elevated viability and no significant homing defects, Itpkb(-/-) HSC had a severely reduced competitive long-term repopulating potential. Aging Itpkb(-/-) mice lost hematopoietic stem and progenitor cells and died with severe anemia. WT HSC normally repopulated Itpkb(-/-) hosts, indicating an HSC-intrinsic Itpkb requirement. Itpkb(-/-) HSC showed reduced colony-forming activity and increased stem-cell-factor activation of the phosphoinositide-3-kinase (PI3K) effectors Akt/mammalian/mechanistic target of rapamycin (mTOR). This was reversed by treatment with the Itpkb product and PI3K/Akt antagonist IP4. Transcriptome changes and biochemistry support mTOR hyperactivity in Itpkb(-/-) HSC. Treatment with the mTOR-inhibitor rapamycin reversed the excessive mTOR signaling and hyperproliferation of Itpkb(-/-) HSC without rescuing colony forming activity. Thus, we propose that Itpkb ensures HSC quiescence and function through limiting cytokine-induced PI3K/mTOR signaling and other mechanisms.
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