Evidence map›Paper›PMID 36293193›Full record

ArticleInternational journal of molecular sciences2022

The Binding of CSL Proteins to Either Co-Activators or Co-Repressors Protects from Proteasomal Degradation Induced by MAPK-Dependent Phosphorylation.

Johannes Fechner, Manuela Ketelhut, Dieter Maier, Anette Preiss, Anja C Nagel

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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  3. 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

5 authors at 1 institution in 1 country.

Johannes FechnerDepartment of General Genetics 190g, University of Hohenheim, Garbenstr. 30, 70599 Stuttgart, Germany.
Manuela KetelhutDepartment of General Genetics 190g, University of Hohenheim, Garbenstr. 30, 70599 Stuttgart, Germany.
Dieter MaierDepartment of General Genetics 190g, University of Hohenheim, Garbenstr. 30, 70599 Stuttgart, Germany.ORCID 0000-0003-4460-0959
Anette PreissDepartment of General Genetics 190g, University of Hohenheim, Garbenstr. 30, 70599 Stuttgart, Germany.ORCID 0000-0002-6410-1586
Anja C NagelDepartment of General Genetics 190g, University of Hohenheim, Garbenstr. 30, 70599 Stuttgart, Germany.ORCID 0000-0002-2733-3249
University of Hohenheim · DE

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Deutsche Forschungsgemeinschaft MA 1328/11-1Deutsche Forschungsgemeinschaft NA 427/5-1NIH HHS P40 OD018537
6 · The paper itself

Abstract

The primary role of Notch is to specify cellular identities, whereby the cells respond to amazingly small changes in Notch signalling activity. Hence, dosage of Notch components is crucial to regulation. Central to Notch signal transduction are CSL proteins: together with respective cofactors, they mediate the activation or the silencing of Notch target genes. CSL proteins are extremely similar amongst species regarding sequence and structure. We noticed that the fly homologue suppressor of hairless (Su(H)) is stabilised in transcription complexes. Using specific transgenic fly lines and HeLa RBPJ

Indexed as

Drosophila ProteinsAnimalsCo-Repressor ProteinsDrosophila melanogasterHumansMicePhosphorylationProtein BindingReceptors, NotchRepressor ProteinsCo-Repressor ProteinsDrosophila ProteinsReceptors, NotchRepressor Proteinsactivator complexCSLdegronMAPKNotch signalling dynamicsproteasomal degradationprotein stabilityrepressor complexsuppressor of hairless

Identifiers

PMID36293193
PMCPMC9604145
OpenAlexW4306385420

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.