Evidence map›Paper›PMID 9343182›Full record

ArticleJournal of virology1997

The adenovirus E3-10.4K/14.5K complex mediates loss of cell surface Fas (CD95) and resistance to Fas-induced apoptosis.

J Shisler, C Yang, B Walter, C F Ware, L R Gooding

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
8.9field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 163 citations in OpenAlex.

  1. Review
  2. Adenoviral E3/49K: CD45-targeted immune evasion and therapeutic potential.Frontiers in cellular and infection microbiology · 2026
    Review
  3. Review
  4. Article
  5. Host-virus interaction and viral evasion.Cell biology international · 2021
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Immune regulation and evasion of Mammalian host cell immunity during viral infection.Indian journal of virology : an official organ of Indian Virological Society · 2013
    Article
  17. Article
  18. Article
  19. Article
  20. Article

4 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

5 authors at 2 institutions in 1 country.

J ShislerDepartment of Microbiology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
C Yang
B Walter
C F Ware
L R Gooding
Emory University · USLa Jolla Institute for Immunology · US

Funding

Lymphotoxin alpha Beta and LIGHT cytokine systemsR37AI033068 · NIAID · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI WARE, CARL F · 2003 to 2012
$4.2M
SURFACE LYMPHOTOXIN A/B COMPLEXESR01AI033068 · NIAID · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI WARE, CARL F · 1994 to 2002
$1.0M
VIRAL PROTEINS THAT INHIBIT TNF CYTOLYSISR01CA058736 · NCI · EMORY UNIVERSITY · PI GOODING, LINDA R · 1994 to 2002
$873k
NCI NIH HHS CA58736NIAID NIH HHS AI33068
6 · The paper itself

Abstract

Cytotoxic T cells use Fas (CD95), a member of the tumor necrosis factor (TNF) receptor superfamily, to eliminate virus-infected cells by activation of the apoptotic pathway for cell death. The adenovirus E3 region encodes several proteins that modify immune defenses, including TNF-dependent cell death, which may allow this virus to establish a persistent infection. Here we show that, as an early event during infection, the adenovirus E3-10.4K/14.5K complex selectively induces loss of Fas surface expression and blocks Fas-induced apoptosis of virus-infected cells. Loss of surface Fas occurs within the first 4 h postinfection and is not due to decreased production of Fas protein. The decrease in surface Fas is distinct from the 10.4K/14.5K-mediated loss of the epidermal growth factor receptor on the same cells, because intracellular stores of Fas are not affected. Further, 10.4K/14.5K, which was previously shown to protect against TNF cytolysis, does not induce a loss of TNF receptor, indicating that this complex mediates more than one function to block host defense mechanisms. These results suggest yet another mechanism by which adenovirus modulates host cytotoxic responses that may contribute to persistent infection by human adenoviruses.

Indexed as

ApoptosisAdenovirus E3 ProteinsAdenoviruses, HumanAnimalsCell CompartmentationCell MembraneDown-RegulationErbB Receptorsfas ReceptorHumansLymphotoxin beta ReceptorMiceReceptors, Tumor Necrosis FactorTime FactorsTumor Cells, CulturedAdenovirus E3 ProteinsErbB Receptorsfas ReceptorLTBR protein, humanLtbr protein, mouseLymphotoxin beta ReceptorReceptors, Tumor Necrosis Factor

Identifiers

PMID9343182
PMCPMC192288
OpenAlexW2099287214

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.