Evidence map›Paper›PMID 33174606›Full record

ArticleBlood2021

UTX maintains the functional integrity of the murine hematopoietic system by globally regulating aging-associated genes.

Yasuyuki Sera, Yuichiro Nakata, Takeshi Ueda, Norimasa Yamasaki, Shuhei Koide, Hiroshi Kobayashi, Ken-Ichiro Ikeda, Kohei Kobatake, Masayuki Iwasaki, Hideaki Oda and 13 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 46 citations in OpenAlex.

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  10. Discovery and structural studies of histone demethylases.Frontiers in epigenetics and epigenomics · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors at 10 institutions in 3 countries.

Yasuyuki SeraHuman Disease Models, Institute of Laboratory Animals, Tokyo Women's Medical University, Tokyo, Japan.
Yuichiro NakataChromatin Dynamics in Stem Cells and Cancer Laboratory, Sylvester Comprehensive Cancer Center, University of Miami, Miami, FL.
Takeshi UedaDepartment of Biochemistry, Faculty of Medicine, Kindai University, Osakasayama, Japan.
Norimasa YamasakiDepartment of Disease Models, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Shuhei KoideDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Hiroshi KobayashiDepartment of Stem Cell Biology, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Ken-Ichiro IkedaDepartment of Disease Models, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Kohei KobatakeDepartment of Disease Models, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Masayuki IwasakiHuman Disease Models, Institute of Laboratory Animals, Tokyo Women's Medical University, Tokyo, Japan.
Hideaki OdaDepartment of Pathology, Tokyo Women's Medical University, Tokyo, Japan.
Linda WolffLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, Bethesda, MD.
Akinori KanaiDepartment of Molecular Oncology, Research Institute for Radiation Biology and Medicine.
Akiko NagamachiDepartment of Molecular Oncology, Research Institute for Radiation Biology and Medicine.
Toshiya InabaDepartment of Molecular Oncology, Research Institute for Radiation Biology and Medicine.
Yusuke SotomaruNatural Science Center for Basic Research and Development, and.
Tatsuo IchinoheDepartment of Hematology and Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Miho KoizumiHuman Disease Models, Institute of Laboratory Animals, Tokyo Women's Medical University, Tokyo, Japan.
Yoshihiko MiyakawaHuman Disease Models, Institute of Laboratory Animals, Tokyo Women's Medical University, Tokyo, Japan.
Zen-Ichiro HondaHealth Care Center and Graduate School of Humanities and Sciences, Institute of Environmental Science for Human Life, Ochanomizu University, Tokyo, Japan; and.
Atsushi IwamaDivision of Stem Cell and Molecular Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Toshio SudaCancer Science Institute of Singapore, National University of Singapore Center for Translational Medicine, Singapore.
Keiyo TakuboDepartment of Stem Cell Biology, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Hiroaki HondaHuman Disease Models, Institute of Laboratory Animals, Tokyo Women's Medical University, Tokyo, Japan.
Tokyo Women's Medical University · JPHiroshima University · JPMolecular Oncology (United States) · USNational Center for Global Health and Medicine · JPThe University of Tokyo · JPKindai University · JPNational Cancer Institute · USNational University of Singapore · SGOchanomizu University · JPSylvester Comprehensive Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic regulation is essential for the maintenance of the hematopoietic system, and its deregulation is implicated in hematopoietic disorders. In this study, UTX, a demethylase for lysine 27 on histone H3 (H3K27) and a component of COMPASS-like and SWI/SNF complexes, played an essential role in the hematopoietic system by globally regulating aging-associated genes. Utx-deficient (UtxΔ/Δ) mice exhibited myeloid skewing with dysplasia, extramedullary hematopoiesis, impaired hematopoietic reconstituting ability, and increased susceptibility to leukemia, which are the hallmarks of hematopoietic aging. RNA-sequencing (RNA-seq) analysis revealed that Utx deficiency converted the gene expression profiles of young hematopoietic stem-progenitor cells (HSPCs) to those of aged HSPCs. Utx expression in hematopoietic stem cells declined with age, and UtxΔ/Δ HSPCs exhibited increased expression of an aging-associated marker, accumulation of reactive oxygen species, and impaired repair of DNA double-strand breaks. Pathway and chromatin immunoprecipitation analyses coupled with RNA-seq data indicated that UTX contributed to hematopoietic homeostasis mainly by maintaining the expression of genes downregulated with aging via demethylase-dependent and -independent epigenetic programming. Of note, comparison of pathway changes in UtxΔ/Δ HSPCs, aged muscle stem cells, aged fibroblasts, and aged induced neurons showed substantial overlap, strongly suggesting common aging mechanisms among different tissue stem cells.

Indexed as

AgingAnimalsCellular SenescenceDNA Breaks, Double-StrandedDNA RepairFemaleGene Expression RegulationGenetic Predisposition to DiseaseHematopoiesisHematopoiesis, ExtramedullaryHematopoietic SystemHistone CodeHistone DemethylasesImmune ReconstitutionJumonji Domain-Containing Histone DemethylasesLeukemia, ExperimentalHistone DemethylasesJumonji Domain-Containing Histone DemethylasesKdm6b protein, mouseReactive Oxygen SpeciesRecombinant ProteinsTranscription FactorsUtx protein, mouse

Identifiers

PMID33174606
PMCPMC7918186
OpenAlexW3105315244

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.