ArticleScientific reports2017
PDK1 plays a vital role on hematopoietic stem cell function.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Mitochondria: the key hub for hematopoietic stem cell homeostasis maintenance and fate determination.Stem cell research & therapy · 2026Review
- Glucose transport dependency defines a therapeutic vulnerability in JAK2V617F-driven myeloproliferative neoplasms.Cell communication and signaling : CCS · 2026Article
- A Microbiota- and IL-15-Dependent Innate-Like B Cell Progenitor Expressing E4BP4.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Silencing METTL3 Stabilizes Atherosclerotic Plaques by Regulating the Phenotypic Transformation of Vascular Smooth Muscle Cells via the miR-375-3p/PDK1 Axis.Cardiovascular drugs and therapy · 2023Article
- A novel small molecule, CU05-1189, targeting the pleckstrin homology domain of PDK1 suppresses VEGF-mediated angiogenesis and tumor growth by blocking the Akt signaling pathway.Frontiers in pharmacology · 2023Article
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- Mechanoregulation in hematopoiesis and hematologic disorders.Current stem cell reports · 2020Article
- Regulation of Hematopoietic Stem Cell Fate and Malignancy.International journal of molecular sciences · 2020Review
- Phospho-inositide-dependent kinase 1 regulates signal dependent translation in megakaryocytes and platelets.Journal of thrombosis and haemostasis : JTH · 2020Article
- [The role of PDK1 in the transition of endothelial to hematopoietic cells].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2018Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
3-Phosphoinositide-dependent protein kinase 1 (PDK1) is a pivotal regulator in the phosphoinositide 3-kinase (PI3K)-Akt signaling pathway that have been shown to play key roles in the functional development of B and T cells via activation of AGC protein kinases during hematopoiesis. However, the role of PDK1 in HSCs has not been fully defined. Here we specifically deleted the PDK1 gene in the hematopoietic system and found that PDK1-deficient HSCs exhibited impaired function and defective lineage commitment abilities. Lack of PDK1 caused HSCs to be less quiescent and to produce a higher number of phenotypic HSCs and fewer progenitors. PDK1-deficient HSCs were also unable to reconstitute the hematopoietic system. Notably, HSC function was more dependent on PDK1 than on mTORC2, which indicates that PDK1 plays a dominant role in the Akt-mediated regulation of HSC function. PDK1-deficient HSCs also exhibited reduced ROS levels, and treatment of PDK1-deficient HSCs with L-butathioninesulfoximine in vitro elevated the low ROS level and promoted colony formation. Therefore, PDK1 appears to contribute to HSC function partially via regulating ROS levels.
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Registered trials
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