Evidence map›Paper›PMID 30385877›Full record

ArticleScientific reports2018

Phosphorylation of the neurogenic transcription factor SOX11 on serine 133 modulates neuronal morphogenesis.

Elli-Anna Balta, Iris Schäffner, Marie-Theres Wittmann, Elisabeth Sock, Felix von Zweydorf, Julia von Wittgenstein, Kathrin Steib, Birgit Heim, Elisabeth Kremmer, Benjamin Martin Häberle and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Role of the CDKL1-SOX11 signaling axis in acute kidney injury.American journal of physiology. Renal physiology · 2024
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Regulation of Adult Neurogenesis in Mammalian Brain.International journal of molecular sciences · 2020
    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

13 authors at 4 institutions in 1 country.

Elli-Anna BaltaInstitute of Biochemistry, Friedrich-Alexander Universität Erlangen-Nürnberg, 91054, Erlangen, Germany.
Iris SchäffnerInstitute of Biochemistry, Friedrich-Alexander Universität Erlangen-Nürnberg, 91054, Erlangen, Germany.
Marie-Theres WittmannInstitute of Biochemistry, Friedrich-Alexander Universität Erlangen-Nürnberg, 91054, Erlangen, Germany.
Elisabeth SockInstitute of Biochemistry, Friedrich-Alexander Universität Erlangen-Nürnberg, 91054, Erlangen, Germany.
Felix von ZweydorfDZNE-German Center for Neurodegenerative Diseases, 72076, Tübingen, Germany.
Julia von WittgensteinInstitute of Biochemistry, Friedrich-Alexander Universität Erlangen-Nürnberg, 91054, Erlangen, Germany.
Kathrin SteibInstitute of Developmental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Birgit HeimUniversity of Tübingen, Institute for Ophthalmic Research, Center for Ophthalmology, 72076, Tübingen, Germany.
Elisabeth KremmerMonoclonal Antibody Core Facility, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Benjamin Martin HäberleInstitute of Biochemistry, Friedrich-Alexander Universität Erlangen-Nürnberg, 91054, Erlangen, Germany.
Marius UeffingUniversity of Tübingen, Institute for Ophthalmic Research, Center for Ophthalmology, 72076, Tübingen, Germany.
Dieter Chichung LieInstitute of Biochemistry, Friedrich-Alexander Universität Erlangen-Nürnberg, 91054, Erlangen, Germany. chi.lie@fau.de.
Christian Johannes GloecknerDZNE-German Center for Neurodegenerative Diseases, 72076, Tübingen, Germany. johannes.gloeckner@dzne.de.ORCID http://orcid.org/0000-0001-6494-6944
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEGerman Center for Neurodegenerative Diseases · DEHelmholtz Zentrum München · DESTZ eyetrial · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intellectual disability gene, Sox11, encodes for a critical neurodevelopmental transcription factor with functions in precursor survival, neuronal fate determination, migration and morphogenesis. The mechanisms regulating SOX11's activity remain largely unknown. Mass spectrometric analysis uncovered that SOX11 can be post-translationally modified by phosphorylation. Here, we report that phosphorylatable serines surrounding the high-mobility group box modulate SOX11's transcriptional activity. Through Mass Spectrometry (MS), co-immunoprecipitation assays and in vitro phosphorylation assays followed by MS we verified that protein kinase A (PKA) interacts with SOX11 and phosphorylates it on S133. In vivo replacement of SoxC factors in developing adult-generated hippocampal neurons with SOX11 S133 phospho-mutants indicated that phosphorylation on S133 modulates dendrite development of adult-born dentate granule neurons, while reporter assays suggested that S133 phosphorylation fine-tunes the activation of select target genes. These data provide novel insight into the control of the critical neurodevelopmental regulator SOX11 and imply SOX11 as a mediator of PKA-regulated neuronal development.

Indexed as

AnimalsCerebellar NucleiCyclic AMP-Dependent Protein KinasesDendritesHippocampusMass SpectrometryMiceMorphogenesisNeurogenesisNeuronsPhosphorylationSerineSOXC Transcription FactorsCyclic AMP-Dependent Protein KinasesSerineSox11 protein, mouseSOXC Transcription Factors

Identifiers

PMID30385877
PMCPMC6212486
OpenAlexW2898106007

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.