Evidence map›Paper›PMID 28202763›Full record

ArticleJournal of virology2017

Inhibition of Vpx-Mediated SAMHD1 and Vpr-Mediated Host Helicase Transcription Factor Degradation by Selective Disruption of Viral CRL4 (DCAF1) E3 Ubiquitin Ligase Assembly.

Hong Wang, Haoran Guo, Jiaming Su, Yajuan Rui, Wenwen Zheng, Wenying Gao, Wenyan Zhang, Zhaolong Li, Guanchen Liu, Richard B Markham and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 26 citations in OpenAlex.

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  11. Association Between Neddylation and Immune Response.Frontiers in cell and developmental biology · 2022
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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

12 authors at 5 institutions in 2 countries.

Hong WangSchool of Life Science, Tianjin University, Tianjin, China.
Haoran GuoFirst Hospital of Jilin University, Institute of Virology and AIDS Research, Changchun, Jilin Province, People's Republic of China.
Jiaming SuThe Second Affiliated Hospital of Zhejiang University School of Medicine, Zhejiang, China.
Yajuan RuiFirst Hospital of Jilin University, Institute of Virology and AIDS Research, Changchun, Jilin Province, People's Republic of China.
Wenwen ZhengFirst Hospital of Jilin University, Institute of Virology and AIDS Research, Changchun, Jilin Province, People's Republic of China.
Wenying GaoFirst Hospital of Jilin University, Institute of Virology and AIDS Research, Changchun, Jilin Province, People's Republic of China.
Wenyan ZhangFirst Hospital of Jilin University, Institute of Virology and AIDS Research, Changchun, Jilin Province, People's Republic of China.
Zhaolong LiFirst Hospital of Jilin University, Institute of Virology and AIDS Research, Changchun, Jilin Province, People's Republic of China.
Guanchen LiuFirst Hospital of Jilin University, Institute of Virology and AIDS Research, Changchun, Jilin Province, People's Republic of China.
Richard B MarkhamDepartment of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.
Wei WeiFirst Hospital of Jilin University, Institute of Virology and AIDS Research, Changchun, Jilin Province, People's Republic of China wwei6@jlu.edu.cn xyu2@jhu.edu.
Xiao-Fang YuSchool of Life Science, Tianjin University, Tianjin, China wwei6@jlu.edu.cn xyu2@jhu.edu.
Jilin University · CNFirst Hospital of Jilin University · CNJohns Hopkins University · USSecond Affiliated Hospital of Zhejiang University · CNTianjin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The lentiviral accessory proteins Vpx and Vpr are known to utilize CRL4 (DCAF1) E3 ligase to induce the degradation of the host restriction factor SAMHD1 or host helicase transcription factor (HLTF), respectively. Selective disruption of viral CRL4 (DCAF1) E3 ligase could be a promising antiviral strategy. Recently, we have determined that posttranslational modification (neddylation) of Cullin-4 is required for the activation of Vpx-CRL4 (DCAF1) E3 ligase. However, the mechanism of Vpx/Vpr-CRL4 (DCAF1) E3 ligase assembly is still poorly understood. Here, we report that zinc coordination is an important regulator of Vpx-CRL4 E3 ligase assembly. Residues in a conserved zinc-binding motif of Vpx were essential for the recruitment of the CRL4 (DCAF1) E3 complex and Vpx-induced SAMHD1 degradation. Importantly, altering the intracellular zinc concentration by treatment with the zinc chelator

Indexed as

Carrier ProteinsCell LineDNA-Binding ProteinsEthylenediaminesG2 Phase Cell Cycle CheckpointsHEK293 CellsHIV-1HIV InfectionsHost-Pathogen InteractionsHumansMonomeric GTP-Binding ProteinsMyeloid CellsProtein Serine-Threonine KinasesProtein Structure, TertiaryReceptors, Interleukin-17SAM Domain and HD Domain-Containing Protein 1Carrier ProteinsDCAF1 protein, humanDNA-Binding ProteinsEthylenediaminesHLTF protein, humanIL17RB protein, humanMonomeric GTP-Binding ProteinsN,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamineProtein Serine-Threonine KinasesReceptors, Interleukin-17SAM Domain and HD Domain-Containing Protein 1SAMHD1 protein, humanTranscription FactorsUbiquitin-Protein LigasesViral Regulatory and Accessory Proteinsvpr Gene Products, Human Immunodeficiency Virusvpr protein, Human immunodeficiency virus 1VPX protein, Simian immunodeficiency virusZinccell cycle arrestCRL4 (DCAF1) E3 ligaseVprVpxzinc binding

Identifiers

PMID28202763
PMCPMC5391453
OpenAlexW2587865257

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.