Evidence map›Paper›PMID 28238085›Full record

ArticleCellular and molecular neurobiology2017

O-GlcNAc Glycosylation of nNOS Promotes Neuronal Apoptosis Following Glutamate Excitotoxicity.

Rongrong Chen, Peipei Gong, Tao Tao, Yilu Gao, Jianhong Shen, Yaohua Yan, Chengwei Duan, Jun Wang, Xiaojuan Liu

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. O-GlcNAcylation in ischemic diseases.Frontiers in pharmacology · 2024
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Nutrient regulation of signaling and transcription.The Journal of biological chemistry · 2019
    Review
  10. Review
  11. Review
  12. The emerging link between O-GlcNAcylation and neurological disorders.Cellular and molecular life sciences : CMLS · 2017
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Rongrong ChenDepartment of Geriatric Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Peipei GongDepartment of Neurosurgery, Comprehensive Surgical Laboratory, Affiliated Hospital of Nantong University, Nantong University, Nantong, Jiangsu, China.
Tao TaoJiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong, 226001, Jiangsu, China.
Yilu GaoDepartment of Neurosurgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Jianhong ShenDepartment of Neurosurgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Yaohua YanDepartment of Neurosurgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Chengwei DuanDepartment of Science and Education, Second People's Hospital of Nantong, Nantong University, Nantong, 226001, Jiangsu, China.
Jun WangDepartment of Geriatric Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China. ntwangjun2016@163.com.
Xiaojuan LiuDepartment of Pathogen Biology, Nantong University, Nantong, 226001, Jiangsu, China. lxj@ntu.edu.cn.
Nantong University · CNAffiliated Hospital of Nantong University · CN

Funding

Nantong science and technology project MS12015056the National Natural Science 81202368the National Natural Science 81371335the National Natural Science 81401013the National Natural Science 81401365
6 · The paper itself

Abstract

Ischemic stroke is a dominant health problem with extremely high rates of mortality and disability. The main mechanism of neuronal injury after stroke is excitotoxicity, during which the activation of neuronal nitric oxide synthase (nNOS) exerts a vital role. However, directly blocking N-methyl-D-aspartate receptors or nNOS can lead to severe undesirable effects since they have crucial physiological functions in the central nervous system. Here, we report that nNOS undergoes O-linked-β-N-acetylglucosamine (O-GlcNAc) modification via interacting with O-GlcNAc transferase, and the O-GlcNAcylation of nNOS remarkably increases during glutamate-induced excitotoxicity. In addition, eliminating the O-GlcNAcylation of nNOS protects neurons from apoptosis during glutamate stimulation by decreasing the formation of nNOS-postsynaptic density protein 95 complexes. Taken together, our data suggest a novel function of the O-GlcNAcylation of nNOS in neuronal apoptosis during glutamate excitotoxicity, suggesting a novel therapy strategy for ischemic stroke.

Indexed as

AcetylglucosamineAnimalsApoptosisGlutamic AcidGlycosylationMaleN-AcetylglucosaminyltransferasesNeuronsNitric Oxide Synthase Type IPC12 CellsRatsRats, Sprague-DawleyAcetylglucosamineGlutamic AcidN-AcetylglucosaminyltransferasesNitric Oxide Synthase Type IO-GlcNAc transferaseUDP-N-acetylglucosamine-peptide beta-N-acetylglucosaminyltransferaseExcitotoxicityNeuronal apoptosisnNOSO-GlcNAc glycosylation

Identifiers

PMID28238085
PMCPMC11482135
OpenAlexW2590141727

What Socratic 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 Socratic graph.