Evidence map›Paper›PMID 25006834›Full record

ArticleCancers2014

Phosphorylation of large T antigen regulates merkel cell polyomavirus replication.

Jason Diaz, Xin Wang, Sabrina H Tsang, Jing Jiao, Jianxin You

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  11. Protein-mediated viral latency is a novel mechanism for Merkel cell polyomavirus persistence.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  12. Review
  13. 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

5 authors at 2 institutions in 1 country.

Jason DiazDepartment of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. jdia@mail.med.upenn.edu.
Xin WangDepartment of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. wangxin2@mail.med.upenn.edu.
Sabrina H TsangDepartment of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. sathw323@mail.med.upenn.edu.
Jing JiaoDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA. jiaoj1@email.chop.edu.
Jianxin YouDepartment of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. jianyou@mail.med.upenn.edu.
University of Pennsylvania · USChildren's Hospital of Philadelphia · US

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Robert H. Vonderheide · 1985 to 2026
$222.3M
Translational Research Support CoreP30ES013508 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI A. Clementina Mesaros · 2006 to 2026
$35.3M
Training In Tumor VirologyT32CA115299 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S. · 2006 to 2021
$4.7M
Merkel cell polyomavirus infection, host response, and viral oncogenic mechanismR01CA187718 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Jianxin You · 2015 to 2026
$3.7M
Mechanism of Brd4-mediated papillomavirus host interactionsR01CA142723 · NCI · UNIVERSITY OF PENNSYLVANIA · PI YOU, JIANXIN · 2010 to 2014
$1.8M
Chromatin structure maintenance and cancerR01CA148768 · NCI · UNIVERSITY OF PENNSYLVANIA · PI YOU, JIANXIN · 2010 to 2014
$1.6M
NCI NIH HHS P30 CA016520NCI NIH HHS R01 CA142723NCI NIH HHS R01 CA148768NCI NIH HHS R01 CA187718NCI NIH HHS T32 CA115299NIEHS NIH HHS P30 ES013508
6 · The paper itself

Abstract

Merkel Cell Polyomavirus (MCPyV) was recently discovered as a novel human polyomavirus that is associated with ~80% of Merkel Cell Carcinomas. The Large Tumor antigen (LT) is an early viral protein which has a variety of functions, including manipulation of the cell cycle and initiating viral DNA replication. Phosphorylation plays a critical regulatory role for polyomavirus LT proteins, but no investigation of MCPyV LT phosphorylation has been performed to date. In this report mass spectrometry analysis reveals three unique phosphorylation sites: T271, T297 and T299. In vivo replication assays confirm that phosphorylation of T271 does not play a role in viral replication, while modification at T297 and T299 have dramatic and opposing effects on LT's ability to initiate replication from the viral origin. We test these mutants for their ability to bind, unwind, and act as a functional helicase at the viral origin. These studies provide a framework for understanding how phosphorylation of LT may dynamically regulate viral replication. Although the natural host cell of MCPyV has not yet been established, this work provides a foundation for understanding how LT activity is regulated and provides tools for better exploring this regulation in both natural host cells and Merkel cells.

Identifiers

PMID25006834
PMCPMC4190550
OpenAlexW2087344424

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.