Evidence map›Paper›PMID 18566412›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

CD73 participates in cellular multiresistance program and protects against TRAIL-induced apoptosis.

Andrey Mikhailov, Alice Sokolovskaya, Gennady G Yegutkin, Hanne Amdahl, Anne West, Hideo Yagita, Riitta Lahesmaa, Linda F Thompson, Sirpa Jalkanen, Dmitry Blokhin and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.4field-weighted citation impact, top 15% 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

35 citing papers in PubMed, 61 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. The Clinical Significance of CD73 in Cancer.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. CD73 Promotes Age-Dependent Accretion of Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2020
    Article
  12. Cell type- and tissue-specific functions of ecto-5'-nucleotidase (CD73).American journal of physiology. Cell physiology · 2019
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

11 authors at 1 institution in 4 countries.

Andrey MikhailovTurku Centre for Biotechnology, University of Turku/Abo Akademi University, Turku, Finland.
Alice Sokolovskaya
Gennady G Yegutkin
Hanne Amdahl
Anne West
Hideo Yagita
Riitta Lahesmaa
Linda F Thompson
Sirpa Jalkanen
Dmitry Blokhin
John E Eriksson
Åbo Akademi University · FI

Funding

The Regulation of Inflammatory Responses by CD73R01AI018220 · NIAID · SCRIPPS CLINIC AND RESEARCH FOUNDATION · PI THOMPSON, LINDA F · 1985 to 2012
$3.1M
NIAID NIH HHS AI18220NIAID NIH HHS R01 AI018220
6 · The paper itself

Abstract

The molecular mechanisms underlying the multiresistant phenotype of leukemic and other cancer cells are incompletely understood. We used expression arrays to reveal differences in the gene expression profiles of an apoptosis-resistant T cell leukemia clone (A4) and normally apoptosis-sensitive parental Jurkat cells. CD73 (ecto-5'-nucleotidase) was the most up-regulated gene in the resistant A4 cell clone. A4 cells displayed CD73 surface expression and significant ecto-5'-nucleotidase activity. The role of CD73 was confirmed by transfection of wild-type CD73 into native Jurkat cells, which led to specific resistance against TRAIL-induced apoptosis, but not other types of apoptosis. The protective role of CD73 was further confirmed by small interfering RNA-mediated down-regulation of CD73, restoring TRAIL sensitivity. CD73-mediated resistance was independent of enzymatic activity of CD73, but was reliant on the anchoring of the protein to the membrane via GPI. We suggest that the inhibition of TRAIL signaling works through interaction of CD73 with death receptor 5, as CD73 and death receptor 5 could be coimmunoprecipitated and were shown to be colocalized in the plasma membrane by confocal microscopy. We propose that CD73 is a component of multiresistance machinery, the transcription of which is activated under selective pressure of the immune system.

Indexed as

Apoptosis5'-NucleotidaseBinding SitesDown-RegulationGlycosylphosphatidylinositolsHumansImmunochemistryJurkat CellsOligonucleotide Array Sequence AnalysisReceptors, TNF-Related Apoptosis-Inducing LigandRNA, Small InterferingTNF-Related Apoptosis-Inducing Ligand5'-NucleotidaseGlycosylphosphatidylinositolsReceptors, TNF-Related Apoptosis-Inducing LigandRNA, Small InterferingTNF-Related Apoptosis-Inducing Ligand

Identifiers

PMID18566412
PMCPMC5584620
OpenAlexW1895156328

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.