Evidence map›Paper›PMID 32690704›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

Human cytomegalovirus protein pUL36: A dual cell death pathway inhibitor.

Alice Fletcher-Etherington, Luis Nobre, Katie Nightingale, Robin Antrobus, Jenna Nichols, Andrew J Davison, Richard J Stanton, Michael P Weekes

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
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  3. Mechanisms and Determinants of CMV Reactivation in Kidney Transplantation.International journal of molecular sciences · 2026
    Review
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  11. A viral necrosome mediates direct RIPK3 activation to promote inflammatory necroptosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    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

8 authors at 3 institutions in 1 country.

Alice Fletcher-EtheringtonCambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 0XY, United Kingdom.ORCID 0000-0001-7313-9247
Luis NobreCambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 0XY, United Kingdom.ORCID 0000-0003-0467-8989
Katie NightingaleCambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 0XY, United Kingdom.ORCID 0000-0001-9958-4699
Robin AntrobusCambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 0XY, United Kingdom.
Jenna NicholsMedical Research Council-University of Glasgow Centre for Virus Research, Glasgow G61 1QH, United Kingdom.ORCID 0000-0003-0093-7170
Andrew J DavisonMedical Research Council-University of Glasgow Centre for Virus Research, Glasgow G61 1QH, United Kingdom.ORCID 0000-0002-4991-9128
Richard J StantonDivision of Infection and Immunity, Cardiff University School of Medicine, Cardiff CF14 4XN, United Kingdom.ORCID 0000-0002-6799-1182
Michael P WeekesCambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 0XY, United Kingdom; mpw1001@cam.ac.uk.ORCID 0000-0003-3196-5545
University of Cambridge · GBMRC University of Glasgow Centre for Virus Research · GBCardiff University · GB

Funding

HCRW_ HS-14-11Medical Research Council MC_UU_12014/3Medical Research Council MR/L008734/1Medical Research Council MR/N013433/1Medical Research Council MR/P001602/1Medical Research Council MR/S00971X/1Wellcome Trust 108070/Z/15/Z
6 · The paper itself

Abstract

Human cytomegalovirus (HCMV) is an important human pathogen and a paradigm of intrinsic, innate, and adaptive viral immune evasion. Here, we employed multiplexed tandem mass tag-based proteomics to characterize host proteins targeted for degradation late during HCMV infection. This approach revealed that mixed lineage kinase domain-like protein (MLKL), a key terminal mediator of cellular necroptosis, was rapidly and persistently degraded by the minimally passaged HCMV strain Merlin but not the extensively passaged strain AD169. The strain Merlin viral inhibitor of apoptosis pUL36 was necessary and sufficient both to degrade MLKL and to inhibit necroptosis. Furthermore, mutation of pUL36 Cys

Indexed as

CytomegalovirusApoptosisCells, CulturedCytomegalovirus InfectionsHumansNecroptosisProtein BindingProteolysisViral ProteinsViral Proteinscell deathhuman cytomegalovirusMLKLnecroptosisprotein degradation

Identifiers

PMID32690704
PMCPMC7414183
OpenAlexW3044264283

What OpenQuestion 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 OpenQuestion graph.