Evidence map›Paper›PMID 26255694›Full record

ArticleCellular immunology2015

Epstein-Barr virus Latent Membrane Protein 2A (LMP2A)-mediated changes in Fas expression and Fas-dependent apoptosis: Role of Lyn/Syk activation.

Ryan Incrocci, Samira Hussain, Amanda Stone, Kathryn Bieging, Lauren A C Alt, Michael J Fay, Michelle Swanson-Mungerson

Open access · greenAbstract read
In one paragraph

Article in Cellular immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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  8. RNA mImmunity, inflammation and disease · 2021
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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

7 authors at 1 institution in 1 country.

Ryan IncrocciChicago College of Osteopathic Medicine, Department of Microbiology and Immunology, 555 31st Street, Downers Grove, IL 60515, USA.
Samira HussainCollege of Health Sciences, Department of Biomedical Sciences, 555 31st Street, Downers Grove, IL 60515, USA.
Amanda StoneChicago College of Osteopathic Medicine, Department of Microbiology and Immunology, 555 31st Street, Downers Grove, IL 60515, USA.
Kathryn BiegingDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Lauren A C AltCollege of Health Sciences, Department of Biomedical Sciences, 555 31st Street, Downers Grove, IL 60515, USA.
Michael J FayCollege of Health Sciences, Department of Biomedical Sciences, 555 31st Street, Downers Grove, IL 60515, USA.
Michelle Swanson-MungersonChicago College of Osteopathic Medicine, Department of Microbiology and Immunology, 555 31st Street, Downers Grove, IL 60515, USA. Electronic address: mswans@midwestern.edu.
Stanford University · US

Funding

Functions of Epstein-Barr Virus LMP2A in LatencyR15CA149690 · NCI · MIDWESTERN UNIVERSITY · PI SWANSON-MUNGERSON, MICHELLE · 2010 to 2010
$219k
NCI NIH HHS 1R15CA149690-01NCI NIH HHS R15 CA149690
6 · The paper itself

Abstract

Epstein-Barr virus Latent Membrane Protein 2A (LMP2A) is expressed in EBV-infected B cells in the germinal center, a site of significant apoptosis induced by engagement of Fas on activated B cells. Signals from the B cell receptor (BCR) protect germinal center B cells from Fas-mediated apoptosis, and since LMP2A is a BCR mimic, we hypothesized that LMP2A would also protect B cells from Fas-mediated apoptosis. Surprisingly, latently-infected human and murine B cell lines expressing LMP2A were more sensitive to Fas-mediated apoptosis, as determined by increases in Annexin-V staining, and cleavage of caspase-8, -3 and PARP. Additional studies show that LMP2A-expressing B cell lines demonstrate a Lyn- and Syk-dependent increase in sensitivity to Fas-mediated apoptosis, due to an LMP2A-dependent enhancement in Fas expression. These findings demonstrate the ability for LMP2A to directly increase a pro-apoptotic molecule and have implications for EBV latency as well as the treatment of EBV-associated malignancies.

Indexed as

AnimalsApoptosisB-LymphocytesCell LineEnzyme Activationfas ReceptorHerpesvirus 4, HumanHumansIntracellular Signaling Peptides and ProteinsMiceMutationProtein-Tyrosine KinasesReceptors, Antigen, B-Cellsrc-Family KinasesSyk KinaseViral Matrix ProteinsEBV-associated membrane antigen, Epstein-Barr virusfas ReceptorIntracellular Signaling Peptides and Proteinslyn protein-tyrosine kinaseProtein-Tyrosine KinasesReceptors, Antigen, B-Cellsrc-Family KinasesSyk KinaseSYK protein, humanSyk protein, mouseViral Matrix ProteinsApoptosisB cell receptor (BCR)B cellsEpstein–Barr virusFas (CD95)Latency Membrane Protein 2A (LMP2A)LynPARPSyk

Identifiers

PMID26255694
PMCPMC4618070
OpenAlexW1060037701

What OpenQuestion holds

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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.