Evidence map›Paper›PMID 37830614›Full record

ArticleCells2023

In Cerebellar Atrophy of 12-Month-Old ATM-Null Mice, Transcriptome Upregulations Concern Most Neurotransmission and Neuropeptide Pathways, While Downregulations Affect Prominently Itpr1, Usp2 and Non-Coding RNA.

Marina Reichlmeir, Júlia Canet-Pons, Gabriele Koepf, Wasifa Nurieva, Ruth Pia Duecker, Claudia Doering, Kathryn Abell, Jana Key, Matthew P Stokes, Stefan Zielen and 3 more

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

Article in Cells, 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
0.6field-weighted citation impact, top 29% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  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

13 authors at 3 institutions in 2 countries.

Marina ReichlmeirGoethe University Frankfurt, University Hospital, Clinic of Neurology, Exp. Neurology, Heinrich Hoffmann Str. 7, 60590 Frankfurt am Main, Germany.ORCID 0000-0002-1551-6865
Júlia Canet-PonsGoethe University Frankfurt, University Hospital, Clinic of Neurology, Exp. Neurology, Heinrich Hoffmann Str. 7, 60590 Frankfurt am Main, Germany.
Gabriele KoepfGoethe University Frankfurt, University Hospital, Clinic of Neurology, Exp. Neurology, Heinrich Hoffmann Str. 7, 60590 Frankfurt am Main, Germany.
Wasifa NurievaTransposition and Genome Engineering, Research Centre of the Division of Hematology, Gene and Cell Therapy, Paul Ehrlich Institute, 63225 Langen, Germany.ORCID 0000-0002-0783-9031
Ruth Pia DueckerDivision of Pediatrics, Pulmonology, Allergology, Infectious Diseases and Gastroenterology, Children's Hospital, University Hospital, Goethe-University, 60590 Frankfurt am Main, Germany.ORCID 0000-0002-1292-648X
Claudia DoeringDr. Senckenberg Institute of Pathology, University Hospital Frankfurt, 60590 Frankfurt am Main, Germany.
Kathryn AbellCell Signaling Technology, Inc., Danvers, MA 01923, USA.
Jana KeyGoethe University Frankfurt, University Hospital, Clinic of Neurology, Exp. Neurology, Heinrich Hoffmann Str. 7, 60590 Frankfurt am Main, Germany.
Matthew P StokesCell Signaling Technology, Inc., Danvers, MA 01923, USA.
Stefan ZielenDivision of Pediatrics, Pulmonology, Allergology, Infectious Diseases and Gastroenterology, Children's Hospital, University Hospital, Goethe-University, 60590 Frankfurt am Main, Germany.
Ralf SchubertDivision of Pediatrics, Pulmonology, Allergology, Infectious Diseases and Gastroenterology, Children's Hospital, University Hospital, Goethe-University, 60590 Frankfurt am Main, Germany.ORCID 0000-0002-7124-0904
Zoltán IvicsTransposition and Genome Engineering, Research Centre of the Division of Hematology, Gene and Cell Therapy, Paul Ehrlich Institute, 63225 Langen, Germany.ORCID 0000-0002-7803-6658
Georg AuburgerGoethe University Frankfurt, University Hospital, Clinic of Neurology, Exp. Neurology, Heinrich Hoffmann Str. 7, 60590 Frankfurt am Main, Germany.
Goethe University Frankfurt · DECell Signaling Technology (United States) · USPaul Ehrlich Institut · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The autosomal recessive disorder Ataxia-Telangiectasia is caused by a dysfunction of the stress response protein, ATM. In the nucleus of proliferating cells, ATM senses DNA double-strand breaks and coordinates their repair. This role explains T-cell dysfunction and tumour risk. However, it remains unclear whether this function is relevant for postmitotic neurons and underlies cerebellar atrophy, since ATM is cytoplasmic in postmitotic neurons. Here, we used ATM-null mice that survived early immune deficits via bone-marrow transplantation, and that reached initial neurodegeneration stages at 12 months of age. Global cerebellar transcriptomics demonstrated that ATM depletion triggered upregulations in most neurotransmission and neuropeptide systems. Downregulated transcripts were found for the ATM interactome component

Indexed as

NeuroblastomaNeurodegenerative DiseasesNeuropeptidesAnimalsAtaxia Telangiectasia Mutated ProteinsAtrophyDNADown-RegulationHumansInfantInositol 1,4,5-Trisphosphate ReceptorsMiceMice, KnockoutRNA, UntranslatedSynaptic TransmissionTranscriptomeAtaxia Telangiectasia Mutated ProteinsATM protein, humanDNAInositol 1,4,5-Trisphosphate ReceptorsItpr1 protein, mouseNeuropeptidesRNA, UntranslatedUbiquitin ThiolesteraseUsp2 protein, mousecerebellar ataxiacytoplasmic ATMsynaptic pathology

Identifiers

PMID37830614
PMCPMC10572167
OpenAlexW4387301634

What Socratic 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 Socratic graph.