Evidence map›Paper›PMID 33586242›Full record

ArticleCell proliferation2021

Nbs1-mediated DNA damage repair pathway regulates haematopoietic stem cell development and embryonic haematopoiesis.

Yu Chen, Jie Sun, Zhenyu Ju, Zhao-Qi Wang, Tangliang Li

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. DNA Damage Responses, the Trump Card of Stem Cells in the Survival Game.Advances in experimental medicine and biology · 2024
    Review
  5. Hematopoietic Stem Cells and the Immune System in Development and Aging.International journal of molecular sciences · 2023
    Review
  6. Article
  7. DNA damage and repair in the hematopoietic system.Acta biochimica et biophysica Sinica · 2022
    Review
  8. Article
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

5 authors at 4 institutions in 2 countries.

Yu ChenInstitute of Aging Research, School of Medicine, Hangzhou Normal University, Hangzhou, China.
Jie SunJiangsu Hansoh Pharmaceutical Group Co., Ltd., Lianyungang, China.
Zhenyu JuInstitute of Aging Research, School of Medicine, Hangzhou Normal University, Hangzhou, China.
Zhao-Qi WangLeibniz Institute on Aging - Fritz Lipmann Institute, Jena, Germany.
Tangliang LiInstitute of Aging Research, School of Medicine, Hangzhou Normal University, Hangzhou, China.ORCID https://orcid.org/0000-0003-0671-9166
Hangzhou Normal University · CNHansoh Pharma (China) · CNLeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DEShandong University · CN

Funding

National Key Research and Development Program of China, Stem Cell and Translational Research 2016YFA0100603National Natural Science Foundation of China 31770871National Natural Science Foundation of China 81571380Natural Science Foundation of Zhejiang Province LY16H080009NHC Key Laboratory of Birth Defect for Research and Prevention (Hunan Provincial Maternal and Child Health Care Hospital, Changsha, China) KF2020005
6 · The paper itself

Abstract

objectivesDNA damages pose threats to haematopoietic stem cells (HSC) maintenance and haematopoietic system homeostasis. Quiescent HSCs in adult mouse bone marrow are resistant to DNA damage, while human umbilical cord blood-derived proliferative HSCs are prone to cell death upon ionizing radiation. Murine embryonic HSCs proliferate in foetal livers and divide symmetrically to generate HSC pool. How murine embryonic HSCs respond to DNA damages is not well-defined. MATERIALS AND

methodsMice models with DNA repair molecule Nbs1 or Nbs1/p53 specifically deleted in embryonic HSCs were generated. FACS analysis, in vitro and in vivo HSC differentiation assays, qPCR, immunofluorescence and Western blotting were used to delineate roles of Nbs1-p53 signaling in HSCs and haematopoietic progenitors.

resultsNbs1 deficiency results in persistent DNA breaks in embryonic HSCs, compromises embryonic HSC development and finally results in mouse perinatal lethality. The persistent DNA breaks in Nbs1 deficient embryonic HSCs render cell cycle arrest, while driving a higher rate of cell death in haematopoietic progenitors. Although Nbs1 deficiency promotes Atm-Chk2-p53 axis activation in HSCs and their progenies, ablation of p53 in Nbs1 deficient HSCs accelerates embryonic lethality.

conclusionsOur study discloses that DNA double-strand repair molecule Nbs1 is essential in embryonic HSC development and haematopoiesis. Persistent DNA damages result in distinct cell fate in HSCs and haematopoietic progenitors. Nbs1 null HSCs tend to be maintained through cell cycle arrest, while Nbs1 null haematopoietic progenitors commit cell death. The discrepancies are mediated possibly by different magnitude of p53 signaling.

Indexed as

AnimalsCell Cycle ProteinsCell DifferentiationDNA-Binding ProteinsDNA DamageDNA RepairHematopoiesisHematopoietic Stem CellsMiceSignal TransductionCell Cycle ProteinsDNA-Binding ProteinsNijmegen breakage syndrome 1 protein, mouseCell fateDNA damage responseHaematopoietic stem cellsNbs1p53

Identifiers

PMID33586242
PMCPMC7941224
OpenAlexW3129553742

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.