Evidence map›Paper›PMID 35972263›Full record

ArticleThe European journal of neuroscience2022

In silico gene expression and pathway analysis of DEK in the human brain across the lifespan.

Allie N Greene, Elizabeth T Nguyen, Aditi Paranjpe, Adam Lane, Lisa M Privette Vinnedge, Matia B Solomon

Open access · greenAbstract read
In one paragraph

Article in The European journal of neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 52% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

6 authors at 3 institutions in 1 country.

Allie N GreeneNeuroscience Graduate Program, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.ORCID 0000-0002-5066-4281
Elizabeth T NguyenDepartment of Psychology, University of Cincinnati, Cincinnati, Ohio, USA.
Aditi ParanjpeDivision of Biomedical Informatics, Bioinformatics Collaborative Services, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Adam LaneDivision of Bone Marrow Transplantation and Immune Deficiency, Cancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Lisa M Privette VinnedgeDivision of Oncology, Cancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.ORCID 0000-0003-2087-4920
Matia B SolomonNeuroscience Graduate Program, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.ORCID 0000-0001-6669-4525
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · USUniversity of Cincinnati Medical Center · US

Funding

PREDOCTORAL TRAINING PROGRAM IN THE NEUROSCIENCEST32NS007453 · NINDS · UNIVERSITY OF CINCINNATI · PI HERMAN, JAMES P · 1997 to 2025
$4.0M
NINDS NIH HHS T32 NS007453
6 · The paper itself

Abstract

DEK, a chromatin-remodelling phosphoprotein, is associated with various functions and biological pathways in the periphery, including inflammation, oncogenesis, DNA repair, and transcriptional regulation. We recently identified an association between DEK loss and central nervous system diseases, such as Alzheimer's. To understand DEK's potential role in disease, it is critical to characterize DEK in healthy human brain to distinguish between neural DEK expression and function in healthy versus diseased states like dementia. We utilized two public databases, BrainCloud and Human Brain Transcriptome, and analysed DEK mRNA expression across the lifespan in learning and memory relevant brain regions. Since DEK loss induces phenotypes associated with brain ageing (e.g., DNA damage and apoptosis), we hypothesized that neural DEK expression may be highest during foetal development and lower in elderly individuals. In agreement with this hypothesis, DEK was most prominently expressed during foetal development in all queried forebrain areas, relative to other ages. Consistent with its roles in the periphery, pathways related to DEK in the brain were associated with cellular proliferation, DNA replication and repair, apoptosis, and inflammation. We also found novel neural development-relevant pathways (e.g., synaptic transmission, neurite outgrowth, and myelination) to be enriched from genes correlated with DEK expression. These findings suggest that DEK is important for human brain development. Overall, we highlight age-related changes in neural DEK expression across the human lifespan and illuminate novel biological pathways associated with DEK that are distinct from normal brain ageing. These findings may further our understanding of how DEK impacts brain function and disease susceptibility.

Indexed as

BrainChromosomal Proteins, Non-HistoneOncogene ProteinsPoly-ADP-Ribose Binding ProteinsAgedGene ExpressionHumansInflammationLongevityChromosomal Proteins, Non-HistoneDEK protein, humanOncogene ProteinsPoly-ADP-Ribose Binding Proteinsageing brainbrainbrain databasesdevelopmentneurodegenerationneurodevelopment

Identifiers

PMID35972263
PMCPMC9730547
OpenAlexW4292183032

What OpenQuestion holds

Textmetadata
LicenceTDM
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.