Evidence map›Paper›PMID 30515991›Full record

ArticleAging cell2019

Amyloid β-induced elevation of O-GlcNAcylated c-Fos promotes neuronal cell death.

Heesun Choi, Chaeyoung Kim, Hyundong Song, Moon-Yong Cha, Hyun Jin Cho, Sung Min Son, Haeng Jun Kim, Inhee Mook-Jung

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

20 citing papers in PubMed, 34 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

8 authors at 1 institution in 1 country.

Heesun ChoiDepartment of Biochemistry and Biomedical Sciences, Seoul National University, College of Medicine, Seoul, Korea.
Chaeyoung KimDepartment of Biochemistry and Biomedical Sciences, Seoul National University, College of Medicine, Seoul, Korea.
Hyundong SongDepartment of Biochemistry and Biomedical Sciences, Seoul National University, College of Medicine, Seoul, Korea.
Moon-Yong ChaDepartment of Biochemistry and Biomedical Sciences, Seoul National University, College of Medicine, Seoul, Korea.
Hyun Jin ChoDepartment of Biochemistry and Biomedical Sciences, Seoul National University, College of Medicine, Seoul, Korea.
Sung Min SonDepartment of Biochemistry and Biomedical Sciences, Seoul National University, College of Medicine, Seoul, Korea.
Haeng Jun KimDepartment of Biochemistry and Biomedical Sciences, Seoul National University, College of Medicine, Seoul, Korea.
Inhee Mook-JungDepartment of Biochemistry and Biomedical Sciences, Seoul National University, College of Medicine, Seoul, Korea.
Seoul National University · KR

Funding

MRC 2012R1A5A2A44671346NRF 2014M3C7A1046047NRF 2015M3C7A1028790NRF 2018R1A2A1A19019062
6 · The paper itself

Abstract

Alzheimer's disease (AD) is an age-related neurodegenerative disease characterized by progressive memory loss resulting from cumulative neuronal cell death. O-linked β-N-acetyl glucosamine (O-GlcNAc) modification of the proteins reflecting glucose metabolism is altered in the brains of patients with AD. However, the link between altered O-GlcNAc modification and neuronal cell death in AD is poorly understood. Here, we examined the regulation of O-GlcNAcylation of c-Fos and the effects of O-GlcNAcylated c-Fos on neuronal cell death during AD pathogenesis. We found that amyloid beta (Aβ)-induced O-GlcNAcylation on serine-56 and 57 of c-Fos was resulted from decreased interaction between c-Fos and O-GlcNAcase and promoted neuronal cell death. O-GlcNAcylated c-Fos increased its stability and potentiated the transcriptional activity through higher interaction with c-Jun, resulting in induction of Bim expression leading to neuronal cell death. Taken together, Aβ-induced O-GlcNAcylation of c-Fos plays an important role in neuronal cell death during the pathogenesis of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBcl-2-Like Protein 11beta-N-AcetylhexosaminidasesCell DeathCell LineGene Expression RegulationGlycosylationHumansMice, TransgenicNeuronsProtein StabilityProto-Oncogene Proteins c-fosRats, Sprague-DawleyTranscription, GeneticAmyloid beta-PeptidesBcl-2-Like Protein 11beta-N-Acetylhexosaminidaseshexosaminidase CProto-Oncogene Proteins c-fosAlzheimer’s diseasec-Fosglucose metabolismneuronal cell deathO-linked β-N-acetyl glucosamine (O-GlcNAc)β-amyloid (Aβ)

Identifiers

PMID30515991
PMCPMC6351842
OpenAlexW2902479462

What OpenQuestion holds

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LicenceCC BY
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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.