Evidence map›Paper›PMID 24292677›Full record

ArticleOncogene2014

YGLF motif in the Kaposi sarcoma herpes virus G-protein-coupled receptor adjusts NF-κB activation and paracrine actions.

S Azzi, S S Smith, J Dwyer, H M Leclair, C Alexia, J K Hebda, N Dupin, N Bidère, J Gavard

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 16 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

S Azzi1] CNRS, UMR8104, Paris, France [2] INSERM, U1016, Paris, France [3] Universite Paris Descartes, Sorbonne Paris Cite, Paris, France.
S S Smith1] CNRS, UMR8104, Paris, France [2] INSERM, U1016, Paris, France [3] Universite Paris Descartes, Sorbonne Paris Cite, Paris, France.
J Dwyer1] CNRS, UMR8104, Paris, France [2] INSERM, U1016, Paris, France [3] Universite Paris Descartes, Sorbonne Paris Cite, Paris, France.
H M Leclair1] CNRS, UMR8104, Paris, France [2] INSERM, U1016, Paris, France [3] Universite Paris Descartes, Sorbonne Paris Cite, Paris, France.
C Alexia1] INSERM, U1014, Hopital Paul Brousse, Villejuif, France [2] Universite Paris-Sud P11, Orsay, France [3] Equipe Labellisee Ligue contre le Cancer, Villejuif, France.
J K Hebda1] CNRS, UMR8104, Paris, France [2] INSERM, U1016, Paris, France [3] Universite Paris Descartes, Sorbonne Paris Cite, Paris, France.
N Dupin1] Universite Paris Descartes, Sorbonne Paris Cite, Paris, France [2] Service de dermatologie, Hopital Cochin-Tarnier, AP-HP, Paris, France.
N Bidère1] INSERM, U1014, Hopital Paul Brousse, Villejuif, France [2] Universite Paris-Sud P11, Orsay, France [3] Equipe Labellisee Ligue contre le Cancer, Villejuif, France.
J Gavard1] CNRS, UMR8104, Paris, France [2] INSERM, U1016, Paris, France [3] Universite Paris Descartes, Sorbonne Paris Cite, Paris, France.
Centre National de la Recherche Scientifique · FRInserm · FRHôpital Paul-Brousse · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kaposi sarcoma (KS) and primary effusion lymphoma (PEL) are two pathologies associated with KS herpes virus (KSHV/HHV-8) infection. KSHV genome contains several oncogenes, among which, the viral G-protein-coupled receptor (vGPCR open reading frame 74) has emerged as a major factor in KS pathogenicity. Indeed, vGPCR is a constitutively active receptor, whose expression is sufficient to drive cell transformation in vitro and tumour development in mice. However, neither the role of vGPCR in KSHV-infected B-lymphocytes nor the molecular basis for its constitutive activation is well understood. Here, we show that vGPCR expression contributes to nuclear factor-κB (NF-κB)-dependent cellular survival in both PEL cells and primary B cells from HIV-negative KS patients. We further identified within vGPCR an AP2 consensus binding motif, Y326GLF, that directs its localization between the plasma membrane and clathrin-coated vesicles. The introduction of a mutation in this site (Y326A) increased NF-κB activity and proinflammatory cytokines production. This correlated with exacerbated morphological rearrangement, migration and proliferation of non-infected monocytes. Collectively, our work raises the possibility that KSHV-infected B-lymphocytes use vGPCR to impact ultimately the immune response and communication within the tumour microenvironment in KSHV-associated pathologies.

Indexed as

Amino Acid MotifsBinding SitesB-LymphocytesCell MembraneCell MovementClathrinCytokinesFlow CytometryHEK293 CellsHeLa CellsHerpesvirus 8, HumanHIV InfectionsHumansInflammationJurkat CellsLeukocytes, MononuclearClathrinCytokinesNF-kappa B p50 SubunitNFKB1 protein, humanReceptors, G-Protein-CoupledRNA, Small Interfering

Identifiers

PMID24292677
OpenAlexW2132659489

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.