Evidence map›Paper›PMID 36118237›Full record

ArticleFrontiers in microbiology2022

Synthetic mimetics assigned a major role to IFNAR2 in type I interferon signaling.

Nele Zoellner, Noémi Coesfeld, Frederik Henry De Vos, Jennifer Denter, Haifeng C Xu, Elena Zimmer, Birgit Knebel, Hadi Al-Hasani, Sofie Mossner, Philipp A Lang and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Structure-function of type I and III interferons.Current opinion in immunology · 2024
    Review
  5. Participation of Single-Nucleotide Variants inPathogens (Basel, Switzerland) · 2023
    Review
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 1 institution in 1 country.

Nele ZoellnerMedical Faculty, Institute of Biochemistry and Molecular Biology II, Heinrich-Heine-University, Düsseldorf, Germany.
Noémi CoesfeldMedical Faculty, Institute of Biochemistry and Molecular Biology II, Heinrich-Heine-University, Düsseldorf, Germany.
Frederik Henry De VosMedical Faculty, Institute of Biochemistry and Molecular Biology II, Heinrich-Heine-University, Düsseldorf, Germany.
Jennifer DenterMedical Faculty, Institute of Molecular Medicine II, Heinrich-Heine-University, Düsseldorf, Germany.
Haifeng C XuMedical Faculty, Institute of Molecular Medicine II, Heinrich-Heine-University, Düsseldorf, Germany.
Elena ZimmerMedical Faculty, Institute of Biochemistry and Molecular Biology II, Heinrich-Heine-University, Düsseldorf, Germany.
Birgit KnebelMedical Faculty, Institute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Heinrich-Heine-University, Düsseldorf, Germany.
Hadi Al-HasaniMedical Faculty, Institute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Heinrich-Heine-University, Düsseldorf, Germany.
Sofie MossnerMedical Faculty, Institute of Biochemistry and Molecular Biology II, Heinrich-Heine-University, Düsseldorf, Germany.
Philipp A LangMedical Faculty, Institute of Molecular Medicine II, Heinrich-Heine-University, Düsseldorf, Germany.
Doreen M FlossMedical Faculty, Institute of Biochemistry and Molecular Biology II, Heinrich-Heine-University, Düsseldorf, Germany.
Jürgen SchellerMedical Faculty, Institute of Biochemistry and Molecular Biology II, Heinrich-Heine-University, Düsseldorf, Germany.
Heinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type I interferons (IFNs) are potent inhibitors of viral replication. Here, we reformatted the natural murine and human type I interferon-α/β receptors IFNAR1 and IFNAR2 into fully synthetic biological switches. The transmembrane and intracellular domains of natural IFNAR1 and IFNAR2 were conserved, whereas the extracellular domains were exchanged by nanobodies directed against the fluorescent proteins Green fluorescent protein (GFP) and mCherry. Using this approach, multimeric single-binding GFP-mCherry ligands induced synthetic IFNAR1/IFNAR2 receptor complexes and initiated STAT1/2 mediated signal transduction

Indexed as

cytokineinterferonnanobodysyntheticvirus

Identifiers

PMID36118237
PMCPMC9480868
OpenAlexW4294170325

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.