Evidence map›Paper›PMID 26311851›Full record

ArticleThe Journal of biological chemistry2015

CD47 Receptor Globally Regulates Metabolic Pathways That Control Resistance to Ionizing Radiation.

Thomas W Miller, David R Soto-Pantoja, Anthony L Schwartz, John M Sipes, William G DeGraff, Lisa A Ridnour, David A Wink, David D Roberts

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

55 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
  2. CD47 stabilizes ROBO2 to regulate glioblastoma progression by preventing ITCH-mediated ubiquitination.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  10. Emerging functions of thrombospondin-1 in immunity.Seminars in cell & developmental biology · 2024
    Review
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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 1 institution in 2 countries.

Thomas W MillerFrom the Laboratory of Pathology and Paradigm Shift Therapeutics, Rockville, Maryland 20852, and.ORCID http://orcid.org/0000-0001-8645-2785
David R Soto-PantojaFrom the Laboratory of Pathology and Departments of Cancer Biology and Hypertension and Vascular Research Center, Wake Forest School of Medicine, Winston-Salem, North Carolina 27157 dsotopan@wakehealth.edu.
Anthony L SchwartzFrom the Laboratory of Pathology and.
John M SipesFrom the Laboratory of Pathology and.
William G DeGraffRadiation Biology Branch, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892.
Lisa A RidnourRadiation Biology Branch, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892.
David A WinkRadiation Biology Branch, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892.
David D RobertsFrom the Laboratory of Pathology and droberts@helix.nih.gov.ORCID http://orcid.org/0000-0002-2481-2981
National Institutes of Health · US

Funding

Cellular Interactions with ThrombospondinZIASC009172 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 2009 to 2024
$17.9M
Redox Mechanism Process of Nos2 and COX2 in Stroma tumor interactionZIABC010898 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WINK, DAVID · 2009 to 2025
$8.6M
Roles of Glycoconjugates and Redox Signaling in Tumor BiologyZIASC009174 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 2009 to 2024
$4.9M
Therapeutic targeting of CD47 regulates tumor cell bioenergetics and mitophagyK22CA181274 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SOTO PANTOJA, DAVID R. · 2015 to 2018
$550k
Intramural NIH HHS ZIA BC010898Intramural NIH HHS ZIA SC009172Intramural NIH HHS ZIA SC009174NCI NIH HHS K22 CA181274PHS HHS ZIASC009172PHS HHS ZIASC009174
6 · The paper itself

Abstract

Modulating tissue responses to stress is an important therapeutic objective. Oxidative and genotoxic stresses caused by ionizing radiation are detrimental to healthy tissues but beneficial for treatment of cancer. CD47 is a signaling receptor for thrombospondin-1 and an attractive therapeutic target because blocking CD47 signaling protects normal tissues while sensitizing tumors to ionizing radiation. Here we utilized a metabolomic approach to define molecular mechanisms underlying this radioprotective activity. CD47-deficient cells and cd47-null mice exhibited global advantages in preserving metabolite levels after irradiation. Metabolic pathways required for controlling oxidative stress and mediating DNA repair were enhanced. Some cellular energetics pathways differed basally in CD47-deficient cells, and the global declines in the glycolytic and tricarboxylic acid cycle metabolites characteristic of normal cell and tissue responses to irradiation were prevented in the absence of CD47. Thus, CD47 mediates signaling from the extracellular matrix that coordinately regulates basal metabolism and cytoprotective responses to radiation injury.

Indexed as

Radiation ToleranceAnimalsCD47 AntigenCitric Acid CycleEnergy MetabolismGene DeletionHomeostasisHumansJurkat CellsMetabolic Networks and PathwaysMetabolomicsMiceNucleotidesOxidative StressPentose Phosphate PathwayCD47 AntigenNucleotidesCD47energeticsglucose metabolismnucleoside/nucleotide metabolismoxidative stressradiation biologyradioprotection

Identifiers

PMID26311851
PMCPMC4598996
OpenAlexW1958420503

What OpenQuestion holds

Textmetadata
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.