Evidence map›Paper›PMID 29850989›Full record

ArticleMolecular neurobiology2019

LPS-Induced Inflammation Abolishes the Effect of DYRK1A on IkB Stability in the Brain of Mice.

Alizée Latour, Yuchen Gu, Nadim Kassis, Fabrice Daubigney, Catherine Colin, Blandine Gausserès, Sandrine Middendorp, Jean-Louis Paul, Valérie Hindié, Jean-Christophe Rain and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Genes · 2021
    Review
  9. Article
  10. Review
  11. Article
  12. Molecular Rescue of Dyrk1A Overexpression Alterations in Mice with FontupInternational journal of molecular sciences · 2020
    Article
  13. Article
  14. 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

15 authors at 7 institutions in 3 countries.

Alizée LatourSorbonne Paris Cité, Biologie Fonctionnelle et Adaptative (BFA), Université Paris Diderot, UMR 8251, 75205, Paris, France.
Yuchen GuSorbonne Paris Cité, Biologie Fonctionnelle et Adaptative (BFA), Université Paris Diderot, UMR 8251, 75205, Paris, France.
Nadim KassisSorbonne Paris Cité, Biologie Fonctionnelle et Adaptative (BFA), Université Paris Diderot, UMR 8251, 75205, Paris, France.
Fabrice DaubigneySorbonne Paris Cité, Biologie Fonctionnelle et Adaptative (BFA), Université Paris Diderot, UMR 8251, 75205, Paris, France.
Catherine ColinInserm U 1127, CNRS UMR 7225, Sorbonne Universités, UPMC Univ Paris 06, UMR S 1127, Institut du Cerveau et de la Moelle épinière, ICM, Paris, France.
Blandine GausserèsSorbonne Paris Cité, Biologie Fonctionnelle et Adaptative (BFA), Université Paris Diderot, UMR 8251, 75205, Paris, France.
Sandrine MiddendorpSorbonne Paris Cité, Biologie Fonctionnelle et Adaptative (BFA), Université Paris Diderot, UMR 8251, 75205, Paris, France.
Jean-Louis PaulAP-HP, Hôpital Européen Georges Pompidou, Service de Biochimie, 75015, Paris, France.
Valérie HindiéHYBRIGENICS Services SAS, Paris, France.
Jean-Christophe RainHYBRIGENICS Services SAS, Paris, France.
Jean-Maurice DelabarSorbonne Paris Cité, Biologie Fonctionnelle et Adaptative (BFA), Université Paris Diderot, UMR 8251, 75205, Paris, France.
Eugene YuChildren's Guild Foundation Down Syndrome Research Program, Department of Cancer Genetics, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY, 14263, USA.
Mariona ArbonesCentro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Barcelona, Spain.
Michel MallatInserm U 1127, CNRS UMR 7225, Sorbonne Universités, UPMC Univ Paris 06, UMR S 1127, Institut du Cerveau et de la Moelle épinière, ICM, Paris, France.
Nathalie JanelSorbonne Paris Cité, Biologie Fonctionnelle et Adaptative (BFA), Université Paris Diderot, UMR 8251, 75205, Paris, France. janel@univ-paris-diderot.fr.ORCID http://orcid.org/0000-0002-4746-8941
Université Paris Cité · FRCentre National de la Recherche Scientifique · FRHybrigenics (France) · FRAssistance Publique – Hôpitaux de Paris · FRCentre for Biomedical Network Research on Rare Diseases · ESDélégation Paris 7 · FRRoswell Park Comprehensive Cancer Center · US

Funding

Fondation Jérôme Lejeune 2017a-1634
6 · The paper itself

Abstract

Down syndrome is characterized by premature aging and dementia with neurological features that mimic those found in Alzheimer's disease. This pathology in Down syndrome could be related to inflammation, which plays a role in other neurodegenerative diseases. We previously found a link between the NFkB pathway, long considered a prototypical proinflammatory signaling pathway, and the dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A). DYRK1A is associated with early onset of Alzheimer's disease in Down syndrome patients. Here, we sought to determine the role of DYRK1A on regulation of the NFkB pathway in the mouse brain. We found that over-expression of Dyrk1A (on a C57BL/6J background) stabilizes IκBα protein levels by inhibition of calpain activity and increases cytoplasmic p65 sequestration in the mouse brain. In contrast, Dyrk1A-deficient mice (on a CD1 background) have decreased IκBα protein levels with an increased calpain activity and decreased cytoplasmic p65 sequestration in the brain. Taken together, our results demonstrate a role of DYRK1A in regulation of the NFkB pathway. However, decreased IκBα and DYRK1A protein levels associated with an increased calpain activity were found in the brains of mice over-expressing Dyrk1A after lipopolysaccharide treatment. Although inflammation induced by lipopolysaccharide treatment has a positive effect on calpastatin and a negative effect on DYRK1A protein level, a positive effect on microglial activation is maintained in the brains of mice over-expressing Dyrk1A.

Indexed as

Alzheimer DiseaseAnimalsBrainCalpainDown SyndromeDyrk KinasesInflammationLipopolysaccharidesMicePhosphorylationProtein Serine-Threonine KinasesProtein-Tyrosine KinasesSignal Transductiontau ProteinsCalpainDyrk KinasesLipopolysaccharidesProtein Serine-Threonine KinasesProtein-Tyrosine Kinasestau ProteinsCalpain activityDown syndromeDYRK1AIkBMouse brainNFkB pathway

Identifiers

PMID29850989
OpenAlexW2806540006

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.