Evidence map›Paper›PMID 29950425›Full record

ArticleJournal of virology2018

Kaposi's Sarcoma-Associated Herpesvirus Nonstructural Membrane Protein pK15 Recruits the Class II Phosphatidylinositol 3-Kinase PI3K-C2α To Activate Productive Viral Replication.

Bizunesh Abere, Naira Samarina, Silvia Gramolelli, Jessica Rückert, Gisa Gerold, Andreas Pich, Thomas F Schulz

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
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  9. Article
  10. Human Protein-l-isoaspartateBiochemistry · 2022
    Article
  11. An Overview of Class II Phosphoinositide 3-Kinases.Current topics in microbiology and immunology · 2022
    Article
  12. Article
  13. Review
  14. Review
  15. Article
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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 2 institutions in 1 country.

Bizunesh AbereInstitute of Virology, Hannover Medical School, Hannover, Germany.
Naira SamarinaInstitute of Virology, Hannover Medical School, Hannover, Germany.
Silvia GramolelliInstitute of Virology, Hannover Medical School, Hannover, Germany.
Jessica RückertInstitute of Virology, Hannover Medical School, Hannover, Germany.
Gisa GeroldInstitute for Experimental Virology, Twincore, Center for Experimental and Clinical Infection Research, Hannover, Germany.
Andreas PichResearch Core Unit Proteomics, Institute of Toxicology, Hannover Medical School, Hannover, Germany.
Thomas F SchulzInstitute of Virology, Hannover Medical School, Hannover, Germany schulz.thomas@mh-hannover.de.ORCID https://orcid.org/0000-0001-8792-5345
Medizinische Hochschule Hannover · DECenter for Experimental and Clinical Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kaposi's sarcoma (KS)-associated herpesvirus (KSHV)/human herpesvirus 8 (HHV-8) causes the angiogenic tumor KS and two B-cell malignancies. The KSHV nonstructural membrane protein encoded by the open reading frame (ORF) K15 recruits and activates several cellular proteins, including phospholipase Cγ1 (PLCγ1), components of the NF-κB pathway, as well as members of the Src family of nonreceptor tyrosine kinases, and thereby plays an important role in the activation of angiogenic and inflammatory pathways that contribute to the pathogenesis of KS as well as KSHV productive (lytic) replication. In order to identify novel cellular components involved in the biology of pK15, we immunoprecipitated pK15 from KSHV-infected endothelial cells and identified associated proteins by label-free quantitative mass spectrometry. Cellular proteins interacting with pK15 point to previously unappreciated cellular processes, such as the endocytic pathway, that could be involved in the function of pK15. We found that the class II phosphatidylinositol 3-kinase (PI3K) PI3K-C2α, which is involved in the endocytosis of activated receptor tyrosine kinases and their signaling from intracellular organelles, interacts and colocalizes with pK15 in vesicular structures abundant in the perinuclear area. Further functional analysis revealed that PI3K-C2α contributes to the pK15-dependent phosphorylation of PLCγ1 and Erk1/2. PI3K-C2α also plays a role in KSHV lytic replication, as evidenced by the reduced expression of the viral lytic genes K-bZIP and ORF45 as well as the reduced release of infectious virus in PI3K-C2α-depleted KSHV-infected endothelial cells. Taken together, our results suggest a role of the cellular PI3K-C2α protein in the functional properties of the KSHV pK15 protein.

Indexed as

DNA ReplicationEndocytosisEndothelial CellsHerpesvirus 8, HumanHumansOpen Reading FramesPhosphatidylinositol 3-KinasesSarcoma, KaposiViral Matrix ProteinsViral ProteinsVirus ActivationVirus LatencyVirus ReplicationPhosphatidylinositol 3-KinasesPIK3C2A protein, humanViral Matrix ProteinsViral ProteinsKSHV-K15lytic replicationPI3K-C2α

Identifiers

PMID29950425
PMCPMC6096797
OpenAlexW2810801515

What OpenQuestion holds

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Registered trials

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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.