Evidence map›Paper›PMID 38305737›Full record

ArticleJournal of cell science2024

The neuronal transcription factor MEIS2 is a calpain-2 protease target.

Tanja Müller, Marina Reichlmeir, Ann-Christin Hau, Ilka Wittig, Dorothea Schulte

Open access · hybridAbstract read
In one paragraph

Article in Journal of cell science, 2024. 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
2.0field-weighted citation impact, top 17% 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, 6 citations in OpenAlex.

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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 2 countries.

Tanja MüllerGoethe University, Faculty of Medicine, University Hospital Frankfurt, Institute of Neurology (Edinger Institute), 60528 Frankfurt, Germany.
Marina ReichlmeirGoethe University, Faculty of Medicine, University Hospital Frankfurt, Institute of Neurology (Edinger Institute), 60528 Frankfurt, Germany.
Ann-Christin HauGoethe University, University Hospital Frankfurt, Dr. Senckenberg Institute of Neurooncology and Institute of Neurology (Edinger Institute), Frankfurt Cancer Institute (FCI), University Cancer Center Frankfurt (UCT), MSNZ Junior Group Translational Neurooncology, 60528 Frankfurt, Germany.
Ilka WittigGoethe University, Faculty of Medicine, Institute for Cardiovascular Physiology, Functional Proteomics, 60590, Frankfurt, Germany.
Dorothea SchulteGoethe University, Faculty of Medicine, University Hospital Frankfurt, Institute of Neurology (Edinger Institute), 60528 Frankfurt, Germany.ORCID 0000-0002-7243-6319
Goethe University Frankfurt · DE

Funding

Deutsche ForschungsgemeinschaftDeutsche Forschungsgemeinschaft SCHU1218/3-3Deutsche KrebshilfeGoethe-Universität Frankfurt am MainPaul and Ursula Klein Foundation
6 · The paper itself

Abstract

Tight control over transcription factor activity is necessary for a sensible balance between cellular proliferation and differentiation in the embryo and during tissue homeostasis by adult stem cells, but mechanistic details have remained incomplete. The homeodomain transcription factor MEIS2 is an important regulator of neurogenesis in the ventricular-subventricular zone (V-SVZ) adult stem cell niche in mice. We here identify MEIS2 as direct target of the intracellular protease calpain-2 (composed of the catalytic subunit CAPN2 and the regulatory subunit CAPNS1). Phosphorylation at conserved serine and/or threonine residues, or dimerization with PBX1, reduced the sensitivity of MEIS2 towards cleavage by calpain-2. In the adult V-SVZ, calpain-2 activity is high in stem and progenitor cells, but rapidly declines during neuronal differentiation, which is accompanied by increased stability of MEIS2 full-length protein. In accordance with this, blocking calpain-2 activity in stem and progenitor cells, or overexpression of a cleavage-insensitive form of MEIS2, increased the production of neurons, whereas overexpression of a catalytically active CAPN2 reduced it. Collectively, our results support a key role for calpain-2 in controlling the output of adult V-SVZ neural stem and progenitor cells through cleavage of the neuronal fate determinant MEIS2.

Indexed as

Neural Stem CellsTranscription FactorsAnimalsCalpainCell DifferentiationCell ProliferationEndopeptidasesHomeodomain ProteinsLateral VentriclesMiceNeurogenesisNeuronsPeptide HydrolasesCalpainCapn2 protein, mouseEndopeptidasesHomeodomain ProteinsMrg1 protein, mousePeptide HydrolasesTranscription FactorsAdult neurogenesisCalpainMEIS homeodomain proteinStem cellSubventricular zoneTranscription factor

Identifiers

PMID38305737
PMCPMC10941658
OpenAlexW4391471823

What OpenQuestion holds

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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.