Evidence map›Paper›PMID 38140597›Full record

ArticleViruses2023

Identification of Adenovirus E1B-55K Interaction Partners through a Common Binding Motif.

Nafiseh Chalabi Hagkarim, Wing-Hang Ip, Luca D Bertzbach, Tareq Abualfaraj, Thomas Dobner, David P Molloy, Grant S Stewart, Roger J Grand

Abstract read
In one paragraph

Article in Viruses, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. 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

8 authors.

Nafiseh Chalabi HagkarimInstitute for Cancer and Genomic Sciences, The Medical School, University of Birmingham, Birmingham B15 2TT, UK.
Wing-Hang IpLeibniz Institute of Virology, Department of Viral Transformation, 20251 Hamburg, Germany.ORCID 0000-0002-5367-1401
Luca D BertzbachLeibniz Institute of Virology, Department of Viral Transformation, 20251 Hamburg, Germany.ORCID 0000-0002-0698-5395
Tareq AbualfarajDepartment of Medical Microbiology and Immunology, Taibah University, P.O. Box 344, Madinah 41477, Saudi Arabia.ORCID 0000-0003-2747-679X
Thomas DobnerLeibniz Institute of Virology, Department of Viral Transformation, 20251 Hamburg, Germany.ORCID 0000-0001-7392-8588
David P MolloyDepartment of Biochemistry and Molecular Biology, School of Basic Medical Science, Chongqing Medical University, Chongqing 400016, China.ORCID 0000-0003-3880-607X
Grant S StewartInstitute for Cancer and Genomic Sciences, The Medical School, University of Birmingham, Birmingham B15 2TT, UK.ORCID 0000-0002-0960-3241
Roger J GrandInstitute for Cancer and Genomic Sciences, The Medical School, University of Birmingham, Birmingham B15 2TT, UK.ORCID 0000-0003-1510-3267

Funding

Bundesministerium für Gesundheit (Federal Ministry of Health) n/aCR-UK Programme Grant C17183/A23303Freie und Hansestadt Hamburg n/aHigh-End Foreign Experts Program of the Ministry of Science and Technology of China G2021035005LUniversity of Birmingham JustGiving scheme n/a
6 · The paper itself

Abstract

The adenovirus C5 E1B-55K protein is crucial for viral replication and is expressed early during infection. It can interact with E4orf6 to form a complex that functions as a ubiquitin E3 ligase. This complex targets specific cellular proteins and marks them for ubiquitination and, predominantly, subsequent proteasomal degradation. E1B-55K interacts with various proteins, with p53 being the most extensively studied, although identifying binding sites has been challenging. To explain the diverse range of proteins associated with E1B-55K, we hypothesized that other binding partners might recognize the simple p53 binding motif (xWxxxPx). In silico analyses showed that many known E1B-55K binding proteins possess this amino acid sequence; therefore, we investigated whether other xWxxxPx-containing proteins also bind to E1B-55K. Our findings revealed that many cellular proteins, including ATR, CHK1, USP9, and USP34, co-immunoprecipitate with E1B-55K. During adenovirus infection, several well-characterized E1B-55K binding proteins and newly identified interactors, including CSB, CHK1, and USP9, are degraded in a cullin-dependent manner. Notably, certain binding proteins, such as ATR and USP34, remain undegraded during infection. Structural predictions indicate no conservation of structure around the proposed binding motif, suggesting that the interaction relies on the correct arrangement of tryptophan and proline residues.

Indexed as

Adenoviridae InfectionsAdenovirus E4 ProteinsAdenoviruses, HumanAdenoviridaeAdenovirus E1B ProteinsHumansTumor Suppressor Protein p53Ubiquitin-Protein LigasesAdenovirus E1B ProteinsAdenovirus E4 ProteinsTumor Suppressor Protein p53Ubiquitin-Protein Ligasesadenoviruscullinearly region 1BMRE11p53p53 binding motifPR619USP

Identifiers

PMID38140597
PMCPMC10747525

What Socratic 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 Socratic graph.