Evidence map›Paper›PMID 23591719›Full record

ArticleScientific reports2013

Thrombospondin-1 signaling through CD47 inhibits self-renewal by regulating c-Myc and other stem cell transcription factors.

Sukhbir Kaur, David R Soto-Pantoja, Erica V Stein, Chengyu Liu, Abdel G Elkahloun, Michael L Pendrak, Alina Nicolae, Satya P Singh, Zuqin Nie, David Levens and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

102 citing papers in PubMed, 138 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Deciphering the role of CD47 in cancer immunotherapy.Journal of advanced research · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

42 more citing papers are in PubMed but not listed here.

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

12 authors at 7 institutions in 2 countries.

Sukhbir KaurLaboratory of Pathology, Center for Cancer Research, National Cancer Institute.
David R Soto-Pantoja
Erica V Stein
Chengyu Liu
Abdel G Elkahloun
Michael L Pendrak
Alina Nicolae
Satya P Singh
Zuqin Nie
David Levens
Jeffrey S Isenberg
David D Roberts
Center for Cancer Research · USCancer Institute (WIA) · INGeorge Washington University · USNational Heart Lung and Blood Institute · USNational Human Genome Research Institute · USNational Institute of Allergy and Infectious Diseases · USUniversity of Pittsburgh · US

Funding

Vascular Subphenotypes of Lung DiseaseP01HL103455 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GLADWIN, MARK T · 2011 to 2020
$26.1M
Transgenic CoreZICHL005907 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI LIU, CHENGYU · 2010 to 2025
$25.8M
Cellular Interactions with ThrombospondinZIASC009172 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 2009 to 2024
$17.9M
NHGRI/DIR Microarray CoreZICHG200365 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI ELKAHLOUN, ABDEL · 2011 to 2025
$9.0M
c-Myc FunctionZIABC011465 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LEVENS, DAVID L. · 2012 to 2025
$8.6M
TSP1-CD47 in Promotion of PAH-Associated Vasoconstriction and Vascular OvergrowthR01HL108954 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ISENBERG, JEFFREY S · 2011 to 2014
$1.4M
Intramural NIH HHSNHLBI NIH HHS 1P01HL103455-01NHLBI NIH HHS 1R01HL108954-01NHLBI NIH HHS P01 HL103455NHLBI NIH HHS R01 HL108954
6 · The paper itself

Abstract

Signaling through the thrombospondin-1 receptor CD47 broadly limits cell and tissue survival of stress, but the molecular mechanisms are incompletely understood. We now show that loss of CD47 permits sustained proliferation of primary murine endothelial cells, increases asymmetric division, and enables these cells to spontaneously reprogram to form multipotent embryoid body-like clusters. c-Myc, Klf4, Oct4, and Sox2 expression is elevated in CD47-null endothelial cells, in several tissues of CD47- and thrombospondin-1-null mice, and in a human T cell line lacking CD47. CD47 knockdown acutely increases mRNA levels of c-Myc and other stem cell transcription factors in cells and in vivo, whereas CD47 ligation by thrombospondin-1 suppresses c-Myc expression. The inhibitory effects of increasing CD47 levels can be overcome by maintaining c-Myc expression and are absent in cells with dysregulated c-Myc. Thus, CD47 antagonists enable cell self-renewal and reprogramming by overcoming negative regulation of c-Myc and other stem cell transcription factors.

Indexed as

AnimalsCD47 AntigenCells, CulturedEndothelial CellsGene Expression RegulationKruppel-Like Factor 4MiceModels, BiologicalProto-Oncogene Proteins c-mycSignal TransductionStem CellsThrombospondin 1Transcription FactorsCD47 AntigenCd47 protein, mouseKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Myc protein, mouseProto-Oncogene Proteins c-mycThrombospondin 1Transcription Factors

Identifiers

PMID23591719
PMCPMC3628113
OpenAlexW1978975562

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.