Evidence map›Paper›PMID 29288703›Full record

ArticleExperimental hematology2018

Loss of DEK induces radioresistance of murine restricted hematopoietic progenitors.

Juana Serrano-Lopez, Kalpana Nattamai, Nicholas A Pease, Miranda S Shephard, Ashley M Wellendorf, Mathieu Sertorio, Eric A Smith, Hartmut Geiger, Susanne I Wells, Jose A Cancelas and 1 more

Open access · greenAbstract read
In one paragraph

Article in Experimental hematology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

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  12. Role of the DEK oncogene in the development of squamous cell carcinoma.International journal of clinical oncology · 2020
    Review
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

11 authors at 2 institutions in 1 country.

Juana Serrano-LopezCancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Kalpana NattamaiCancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Nicholas A PeaseCancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Miranda S ShephardCancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Ashley M WellendorfCancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Mathieu SertorioCancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Eric A SmithCancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Hartmut GeigerCancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Susanne I WellsCancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Jose A CancelasCancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Lisa M Privette VinnedgeCancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio. Electronic address: Lisa.Privette@cchmc.org.
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati Medical Center · US

Funding

Medical Scientist Training ProgramT32GM063483 · NIGMS · UNIVERSITY OF CINCINNATI · PI KHURANA HERSHEY, GURJIT K. · 2002 to 2022
$6.7M
Ohio Interdisciplinary Women's Health Career TrainingK12HD051953 · NICHD · UNIVERSITY OF CINCINNATI · PI TSEVAT, JOEL · 2005 to 2014
$4.2M
Cincinnati Center for Excellence in Molecular HematologyP30DK090971 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2010 to 2015
$4.0M
Role and Regulaton of the Human DEK Proto-OncogeneR01CA116316 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI WELLS, SUSANNE I · 2006 to 2016
$2.9M
Cdc42, hematopoietic stem cell polarity, and cell fateR01DK104814 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2016 to 2019
$2.0M
Lineage Determination and Tissue HomeOstasis in the aged Hematopoietic SystemR01AG040118 · NIA · CINCINNATI CHILDRENS HOSP MED CTR · PI GEIGER, HARTMUT, ZHENG, YI · 2011 to 2015
$1.7M
G-CSF in Human Severe Congenital NeutropeniaR01GM110628 · NIGMS · CINCINNATI CHILDRENS HOSP MED CTR · PI CANCELAS, JOSE A., LUTZKO, CAROLYN M · 2015 to 2018
$1.2M
Stem cell aging and biomarker studiesR56AG050650 · NIA · CINCINNATI CHILDRENS HOSP MED CTR · PI GEIGER, HARTMUT, ZHENG, YI · 2015 to 2015
$390k
NCI NIH HHS R01 CA116316NIA NIH HHS R01 AG040118NIA NIH HHS R56 AG050650NICHD NIH HHS K12 HD051953NIDDK NIH HHS P30 DK090971NIDDK NIH HHS R01 DK104814NIGMS NIH HHS R01 GM110628NIGMS NIH HHS T32 GM063483
6 · The paper itself

Abstract

Self-renewing hematopoietic stem cells and multipotent progenitor cells are responsible for maintaining hematopoiesis throughout an individual's lifetime. For overall health and survival, it is critical that the genome stability of these cells is maintained and that the cell population is not exhausted. Previous reports have indicated that the DEK protein, a chromatin structural protein that functions in numerous nuclear processes, is required for DNA damage repair in vitro and long-term engraftment of hematopoietic stem cells in vivo. Therefore, we investigated the role of DEK in normal hematopoiesis and response to DNA damaging agents in vivo. Here, we report that hematopoiesis is largely unperturbed in DEK knockout mice compared with wild-type (WT) controls. However, DEK knockout mice have fewer radioprotective units, but increased capacity to survive repeated sublethal doses of radiation exposure compared with WT mice. Furthermore, this increased survival correlated with a sustained quiescent state in which DEK knockout restricted hematopoietic progenitor cells (HPC-1) were nearly three times more likely to be quiescent following irradiation compared with WT cells and were significantly more radioresistant during the early phases of myeloid reconstitution. Together, our studies indicate that DEK functions in the normal hematopoietic stress response to recurrent radiation exposure.

Indexed as

DNA DamageAnimalsDNA-Binding ProteinsHematopoiesisHematopoietic Stem CellsMiceMice, KnockoutOncogene ProteinsPoly-ADP-Ribose Binding ProteinsRadiation ToleranceDEK protein, mouseDNA-Binding ProteinsOncogene ProteinsPoly-ADP-Ribose Binding Proteins

Identifiers

PMID29288703
PMCPMC5844846
OpenAlexW2777629316

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.