Evidence map›Paper›PMID 28081176›Full record

ArticlePloS one2017

Radiation Induced Apoptosis of Murine Bone Marrow Cells Is Independent of Early Growth Response 1 (EGR1).

Karine Z Oben, Beth W Gachuki, Sara S Alhakeem, Mary K McKenna, Ying Liang, Daret K St Clair, Vivek M Rangnekar, Subbarao Bondada

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 pooled it
1.6field-weighted citation impact, top 17% 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, 2 syntheses or guidelines pooled it, 61 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Karine Z ObenDepartment of Microbiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, Kentucky, United States of America.
Beth W GachukiDepartment of Microbiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, Kentucky, United States of America.
Sara S AlhakeemDepartment of Microbiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, Kentucky, United States of America.
Mary K McKennaDepartment of Microbiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, Kentucky, United States of America.
Ying LiangDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, Kentucky, United States of America.
Daret K St ClairDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, Kentucky, United States of America.
Vivek M RangnekarDepartment of Microbiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, Kentucky, United States of America.
Subbarao BondadaDepartment of Microbiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, Kentucky, United States of America.
University of Kentucky · USMarkey Cancer Center · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
Latexin function in the maintenance and regeneration of the hematopoietic systemR01HL124015 · NHLBI · UNIVERSITY OF KENTUCKY · PI LIANG, YING · 2016 to 2024
$3.6M
Role of Tcl1 and Par-4 in regulation of chronic lymphocytic leukemiaR01CA165469 · NCI · UNIVERSITY OF KENTUCKY · PI BONDADA, SUBBARAO, RANGNEKAR, VIVEK M · 2013 to 2017
$1.9M
NCI NIH HHS P30 CA177558NCI NIH HHS R01 CA165469NHLBI NIH HHS R01 HL124015
6 · The paper itself

Abstract

An understanding of how each individual 5q chromosome critical deleted region (CDR) gene contributes to malignant transformation would foster the development of much needed targeted therapies for the treatment of therapy related myeloid neoplasms (t-MNs). Early Growth Response 1 (EGR1) is a key transcriptional regulator of myeloid differentiation located within the 5q chromosome CDR that has been shown to regulate HSC (hematopoietic stem cell) quiescence as well as the master regulator of apoptosis-p53. Since resistance to apoptosis is a hallmark of malignant transformation, we investigated the role of EGR1 in apoptosis of bone marrow cells; a cell population from which myeloid malignancies arise. We evaluated radiation induced apoptosis of Egr1+/+ and Egr1-/- bone marrow cells in vitro and in vivo. EGR1 is not required for radiation induced apoptosis of murine bone marrow cells. Neither p53 mRNA (messenger RNA) nor protein expression is regulated by EGR1 in these cells. Radiation induced apoptosis of bone marrow cells by double strand DNA breaks induced p53 activation. These results suggest EGR1 dependent signaling mechanisms do not contribute to aberrant apoptosis of malignant cells in myeloid malignancies.

Indexed as

Radiation, IonizingAnimalsApoptosisBone Marrow CellsCells, CulturedDNA Breaks, Double-StrandedEarly Growth Response Protein 1HistonesMiceMicroscopy, FluorescenceReal-Time Polymerase Chain ReactionRNA, MessengerTibiaTumor Suppressor Protein p53Up-RegulationWhole-Body IrradiationEarly Growth Response Protein 1Egr1 protein, mousegamma-H2AX protein, mouseHistonesRNA, MessengerTumor Suppressor Protein p53

Identifiers

PMID28081176
PMCPMC5230770
OpenAlexW2579476886

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.