Evidence map›Paper›PMID 34686927›Full record

ArticleGlycoconjugate journal2021

Sialidase neu4 deficiency is associated with neuroinflammation in mice.

Zehra Kevser Timur, Orhan Kerim Inci, Secil Akyildiz Demir, Volkan Seyrantepe

Abstract read
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In one paragraph

Article in Glycoconjugate journal, 2021. 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
0.3field-weighted citation impact, top 43% 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, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Targeting Neuraminidase 4 Attenuates Kidney Fibrosis in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  4. Review
  5. 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

4 authors at 1 institution in 1 country.

Zehra Kevser TimurDepartment of Molecular Biology and Genetics, Izmir Institute of Technology, Urla, Izmir, Turkey.
Orhan Kerim InciDepartment of Molecular Biology and Genetics, Izmir Institute of Technology, Urla, Izmir, Turkey.
Secil Akyildiz DemirIzmir Institute of Technology, IYTEDEHAM, Urla, İzmir, Turkey.
Volkan SeyrantepeDepartment of Molecular Biology and Genetics, Izmir Institute of Technology, Urla, Izmir, Turkey. volkanseyrantepe@iyte.edu.tr.
Izmir Institute of Technology · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sialidases catalyze the removal of sialic acid residues from glycoproteins, oligosaccharides, and sialylated glycolipids. Sialidase Neu4 is in the lysosome and has broad substrate specificity. Previously generated Neu4-/- mice were viable, fertile and lacked gross morphological abnormalities, but displayed a marked vacuolization and lysosomal storage in lung and spleen cells. In addition, we showed that there is an increased level of GD1a ganglioside and a markedly decreased level of GM1 ganglioside in the brain of Neu4-/- mice. In this study, we further explored whether sialidase Neu4 deficiency causes neuroinflammation. We demostrated that elevated level of GD1a and GT1b is associated with an increased level of LAMP1-positive lysosomal vesicles and Tunel-positive neurons correlated with alterations in the expression of cytokines and chemokines in adult Neu4-/- mice. Astrogliosis and microgliosis were also significantly enhanced in the hippocampus, and cerebellum. These changes in brain immunity were accompanied by motor impairment in these mice. Our results indicate that sialidase Neu4 is a novel mediator of an inflammatory response in the mouse brain due to the altered catabolism of gangliosides.

Indexed as

MucolipidosesAnimalsGangliosidesLysosomesMiceNeuraminidaseNeuroinflammatory DiseasesSubstrate SpecificityGangliosidesNeu4 protein, mouseNeuraminidaseBehaviorGangliosideNeu4NeuroinflammationSialidase

Identifiers

PMID34686927
OpenAlexW3205224532

What OpenQuestion holds

Textmetadata
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.