Evidence map›Paper›PMID 24699724›Full record

ArticlePLoS pathogens2014

Efficient parvovirus replication requires CRL4Cdt2-targeted depletion of p21 to prevent its inhibitory interaction with PCNA.

Richard O Adeyemi, Matthew S Fuller, David J Pintel

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 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
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

15 citing papers in PubMed, 21 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

3 authors at 1 institution in 1 country.

Richard O AdeyemiDepartment of Molecular Microbiology and Immunology, C.S. Bond Life Sciences Center, University of Missouri-Columbia, School of Medicine, Columbia, Missouri, United States of America.
Matthew S FullerDepartment of Molecular Microbiology and Immunology, C.S. Bond Life Sciences Center, University of Missouri-Columbia, School of Medicine, Columbia, Missouri, United States of America.
David J PintelDepartment of Molecular Microbiology and Immunology, C.S. Bond Life Sciences Center, University of Missouri-Columbia, School of Medicine, Columbia, Missouri, United States of America.
University of Missouri · US

Funding

Parvovirus RNA Processing and Gene Expression StrategiesR01AI046458 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI PINTEL, DAVID J. · 2000 to 2018
$4.6M
Parvovirus-Cell InteractionsR01AI091588 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI PINTEL, DAVID J. · 2011 to 2015
$1.5M
Parvovirus RNA Processing and Gene Expression StrategiesR56AI046458 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI PINTEL, DAVID J. · 2013 to 2013
$374k
NIAID NIH HHS AI 46458NIAID NIH HHS AI 91588NIAID NIH HHS R01 AI046458NIAID NIH HHS R01 AI091588NIAID NIH HHS R56 AI046458
6 · The paper itself

Abstract

Infection by the autonomous parvovirus minute virus of mice (MVM) induces a vigorous DNA damage response in host cells which it utilizes for its efficient replication. Although p53 remains activated, p21 protein levels remain low throughout the course of infection. We show here that efficient MVM replication required the targeting for degradation of p21 during this time by the CRL4Cdt2 E3-ubiquitin ligase which became re-localized to MVM replication centers. PCNA provides a molecular platform for substrate recognition by the CRL4Cdt2 E3-ubiquitin ligase and p21 targeting during MVM infection required its interaction both with Cdt2 and PCNA. PCNA is also an important co-factor for MVM replication which can be antagonized by p21 in vitro. Expression of a stable p21 mutant that retained interaction with PCNA inhibited MVM replication, while a stable p21 mutant which lacked this interaction did not. Thus, while interaction with PCNA was important for targeting p21 to the CRL4Cdt2 ligase re-localized to MVM replication centers, efficient viral replication required subsequent depletion of p21 to abrogate its inhibition of PCNA.

Indexed as

AnimalsCell LineCyclin-Dependent Kinase Inhibitor p21HumansMiceMinute Virus of MiceMutationNuclear ProteinsParvoviridae InfectionsProliferating Cell Nuclear AntigenUbiquitin-Protein LigasesVirus ReplicationCDKN1A protein, humanCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21DTL protein, humanNuclear ProteinsProliferating Cell Nuclear AntigenUbiquitin-Protein Ligases

Identifiers

PMID24699724
PMCPMC3974872
OpenAlexW2082585003

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.