Evidence map›Paper›PMID 26929373›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Endolysosomal trafficking of viral G protein-coupled receptor functions in innate immunity and control of viral oncogenesis.

Xiaonan Dong, Adam Cheng, Zhongju Zou, Yih-Sheng Yang, Rhea M Sumpter, Chou-Long Huang, Govind Bhagat, Herbert W Virgin, Sergio A Lira, Beth Levine

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Guideline
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  7. Article
  8. Review
  9. Article
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  11. Article
  12. Review
  13. Autophagy and Viral Infection.Advances in experimental medicine and biology · 2019
    Review
  14. Review
  15. Article
  16. BECN2 interacts with ATG14 through a metastable coiled-coil to mediate autophagy.Protein science : a publication of the Protein Society · 2017
    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

10 authors at 5 institutions in 1 country.

Xiaonan DongDepartment of Internal Medicine, Center for Autophagy Research, University of Texas Southwestern Medical Center, Dallas, TX 75390;
Adam ChengDepartment of Internal Medicine, Center for Autophagy Research, University of Texas Southwestern Medical Center, Dallas, TX 75390;
Zhongju ZouDepartment of Internal Medicine, Center for Autophagy Research, University of Texas Southwestern Medical Center, Dallas, TX 75390; Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390;
Yih-Sheng YangDivision of Nephrology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390;
Rhea M SumpterDepartment of Internal Medicine, Center for Autophagy Research, University of Texas Southwestern Medical Center, Dallas, TX 75390;
Chou-Long HuangDivision of Nephrology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390;
Govind BhagatDepartment of Pathology and Cell Biology, Columbia University Medical Center and New York Presbyterian Hospital, New York, NY 10032;
Herbert W VirginDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110;
Sergio A LiraImmunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029;
Beth LevineDepartment of Internal Medicine, Center for Autophagy Research, University of Texas Southwestern Medical Center, Dallas, TX 75390; Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390; Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390 beth.levine@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · USHoward Hughes Medical Institute · USIcahn School of Medicine at Mount Sinai · USNew York Hospital Queens · USWashington University in St. Louis · US

Funding

Genetic and Pathway Analysis CoreU19AI109725 · NIAID · WASHINGTON UNIVERSITY · PI ALLEN, PAUL M · 2014 to 2018
$32.7M
UT Southwestern O'Brien Kidney Research Core CenterP30DK079328 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MOE, ORSON W · 2007 to 2021
$16.9M
TRAINING PROGRAM IN IMMUNOLOGY AND IMMUNOGENETICST32AI007163 · NIAID · WASHINGTON UNIVERSITY · PI Kenneth M Murphy, Kodi S Ravichandran · 1985 to 2026
$14.8M
THE ROLE OF ICSBP IN MUCOSAL IMMUNE RESPONSEP01DK072201 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HARPAZ, NOAM · 2006 to 2015
$14.6M
Molecular pathogenesis of intestinal serrated polypsR01CA161373 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LIRA, SERGIO A. · 2011 to 2020
$3.7M
Beclin 1-Bcl-2 Interactions: Effects on AutophagyR01CA109618 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI LEVINE, BETH C · 2004 to 2014
$3.1M
Novel host factors in selective autophagy of virusesK08AI099150 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI SUMPTER, RHEA M · 2012 to 2014
$391k
Howard Hughes Medical InstituteNCI NIH HHS R01 CA109618NCI NIH HHS R01 CA161373NIAID NIH HHS K08 AI099150NIAID NIH HHS T32 AI007163NIAID NIH HHS U19 AI109725NIDDK NIH HHS P01 DK072201NIDDK NIH HHS P30 DK079328
6 · The paper itself

Abstract

The ubiquitin-proteasome system degrades viral oncoproteins and other microbial virulence factors; however, the role of endolysosomal degradation pathways in these processes is unclear. Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi's sarcoma, and a constitutively active viral G protein-coupled receptor (vGPCR) contributes to the pathogenesis of KSHV-induced tumors. We report that a recently discovered autophagy-related protein, Beclin 2, interacts with KSHV GPCR, facilitates its endolysosomal degradation, and inhibits vGPCR-driven oncogenic signaling. Furthermore, monoallelic loss of Becn2 in mice accelerates the progression of vGPCR-induced lesions that resemble human Kaposi's sarcoma. Taken together, these findings indicate that Beclin 2 is a host antiviral molecule that protects against the pathogenic effects of KSHV GPCR by facilitating its endolysosomal degradation. More broadly, our data suggest a role for host endolysosomal trafficking pathways in regulating viral pathogenesis and oncogenic signaling.

Indexed as

AnimalsApoptosis Regulatory ProteinsAutophagyBeclin-1Cell Transformation, ViralCrosses, GeneticDisease Models, AnimalEndocytosisGenetic Predisposition to DiseaseHEK293 CellsHerpesvirus 8, HumanHeterozygoteHumansImmunity, InnateIntercellular Signaling Peptides and ProteinsInterleukin-6Apoptosis Regulatory ProteinsBeclin-1Becn1 protein, mouseIL6 protein, humanIntercellular Signaling Peptides and ProteinsInterleukin-6NF-kappa BORF74 protein, Human herpesvirus 8ProteinsReceptors, ChemokineReceptors, G-Protein-CoupledRNA, Small InterferingViral ProteinsWFIKKN2 protein, humanautophagyBeclin 2endolysosomal traffickingoncogenesisviral GPCR

Identifiers

PMID26929373
PMCPMC4801257
OpenAlexW2292056157

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.