Evidence map›Paper›PMID 17582000›Full record

ArticleJournal of virology2007

Epstein-Barr virus latent membrane protein 2A mediates transformation through constitutive activation of the Ras/PI3-K/Akt Pathway.

Makoto Fukuda, Richard Longnecker

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.

  1. Pooled it
  2. Molecular pathogenesis and evolving treatment landscape of extranodal NK/T-cell lymphoma.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2026
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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

2 authors at 1 institution in 1 country.

Makoto FukudaDepartment of Microbiology-Immunology, Northwestern University Medical School, 303 E. Chicago Ave., Chicago, IL 60611, USA.
Richard Longnecker
Northwestern University · US

Funding

In Vivo Model of Epstein-Barr Virus LatencyR01CA073507 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LONGNECKER, RICHARD M · 1997 to 2018
$6.1M
EBV LATENT MEMBRANE PROTEIN 2R01CA062234 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LONGNECKER, RICHARD M · 1994 to 2007
$2.2M
Functional Studies of gp42 and HLA Class 11 in EBVR01CA093444 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LONGNECKER, RICHARD M · 2002 to 2006
$1.8M
NCI NIH HHS CA62234NCI NIH HHS CA73507NCI NIH HHS CA93444NCI NIH HHS R01 CA062234NCI NIH HHS R01 CA073507NCI NIH HHS R01 CA093444
6 · The paper itself

Abstract

Epstein-Barr virus (EBV) latent membrane protein 2A (LMP2A) is widely expressed in EBV-infected cells within the infected human host and EBV-associated malignancies, suggesting that LMP2A is important for EBV latency, persistence, and EBV-associated tumorigenesis. Previously, we demonstrated that LMP2A provides an antiapoptotic signal through the activation of phosphatidylinositol 3-kinase (PI3-K)/Akt pathway in vitro. However, the exact function of LMP2A in tumor progression is not well understood. In this study, we found that LMP2A did not induce anchorage-independent cell growth in a human keratinocyte cell line, HaCaT, but did in a human gastric carcinoma cell line, HSC-39. In addition, LMP2A activated the PI3-K/Akt pathway in both HaCaT and HSC-39 cells; however, LMP2A did not activate Ras in HaCaT cells but did in HSC-39 cells. Furthermore, the Ras inhibitors manumycin A and a dominant-negative form of Ras (RasN17) and the PI3-K inhibitor LY294002 blocked LMP2A-mediated Akt phosphorylation and anchorage-independent cell growth in HSC-39 cells. These results suggest that constitutive activation of the Ras/PI3-K/Akt pathway by LMP2A is a key factor for LMP2A-mediated transformation.

Indexed as

Cell LineCell Line, TumorCell ProliferationCell Transformation, ViralChromonesEnzyme InhibitorsGene Expression RegulationHerpesvirus 4, HumanHumansKeratinocytesMorpholinesOncogene Protein v-aktPhosphatidylinositol 3-KinasesPolyenesPolyunsaturated Alkamidesras Proteins2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesEBV-associated membrane antigen, Epstein-Barr virusEnzyme InhibitorsmanumycinMorpholinesOncogene Protein v-aktPhosphatidylinositol 3-KinasesPolyenesPolyunsaturated Alkamidesras ProteinsViral Matrix Proteins

Identifiers

PMID17582000
PMCPMC1951437
OpenAlexW2150357985

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.