ArticleOncotarget2016
Evidence that hematopoietic stem cell function is preserved during aging in long-lived S6K1 mutant mice.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Ribosomal S6 kinase 1 regulates inflammaging via the senescence secretome.Nature aging · 2024Article
- The parasitic worm product ES-62 protects the osteoimmunology axis in a mouse model of obesity-accelerated ageing.Frontiers in immunology · 2022Article
- Next Generation Strategies for Geroprotection via mTORC1 Inhibition.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Review
- The Cross-Talk Between Sphingolipids and Insulin-Like Growth Factor Signaling: Significance for Aging and Neurodegeneration.Molecular neurobiology · 2019Review
- mTOR as a central regulator of lifespan and aging.F1000Research · 2019Review
- The role of mTOR-mediated signals during haemopoiesis and lineage commitment.Biochemical Society transactions · 2018Review
- mTOR signaling in stem and progenitor cells.Development (Cambridge, England) · 2018Review
- Rapamycin, proliferation and geroconversion to senescence.Cell cycle (Georgetown, Tex.) · 2018Article
- While reinforcing cell cycle arrest, rapamycin and Torins suppress senescence in UVA-irradiated fibroblasts.Oncotarget · 2017Article
- Prolonged Growth Hormone/Insulin/Insulin-like Growth Factor Nutrient Response Signaling Pathway as a Silent Killer of Stem Cells and a Culprit in Aging.Stem cell reviews and reports · 2017Review
- From rapalogs to anti-aging formula.Oncotarget · 2017Review
- DNA damage-induced phosphatase Wip1 in regulation of hematopoiesis, immune system and inflammation.Cell death discovery · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanistic target of rapamycin (mTOR) signalling pathway plays a highly conserved role in aging; mice lacking ribosomal protein S6 kinase 1 (S6K1-/-) have extended lifespan and healthspan relative to wild type (WT) controls. Exactly how reduced mTOR signalling induces such effects is unclear, although preservation of stem cell function may be important. We show, using gene expression analyses, that there was a reduction in expression of cell cycle genes in young (12 week) and aged (80 week) S6K1-/- BM-derived c-Kit+ cells when compared to age-matched WT mice, suggesting that these cells are more quiescent in S6K1-/- mice. In addition, we investigated hematopoietic stem cell (HSC) frequency and function in young and aged S6K1-/-and WT mice. Young, but not aged, S6K1-/-mice had more LSK (lineage-, c-Kit+, Sca-1+) cells (% of bone marrow (BM)), including the most primitive long-term repopulating HSCs (LT-HSC) relative to WT controls. Donor-derived engraftment of LT-HSCs in recipient mice was unaffected by genotype in young mice, but was enhanced in transplants using LT-HSCs derived from aged S6K1-/- mice. Our results are the first to provide evidence that age-associated HSC functional decline is ameliorated in a long-lived mTOR mutant mouse.
Indexed as
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What OpenQuestion holds
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.