Evidence map›Paper›PMID 25221472›Full record

ReviewFrontiers in cellular neuroscience2014

Mechanisms of NOS1AP action on NMDA receptor-nNOS signaling.

Michael J Courtney, Li-Li Li, Yvonne Y Lai

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Sigma-1 Receptor Activation by Fluvoxamine Ameliorates ER Stress, Synaptic Dysfunction and Behavioral Deficits in a Ketamine Model of Schizophrenia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. An in vitro model of neuronal ensembles.Nature communications · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Nitric Oxide Synthase Inhibitors into the Clinic at Last.Handbook of experimental pharmacology · 2021
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. NOS1AP genetic variation is associated with impaired healing of diabetic foot ulcers and diminished response to healing of circulating stem/progenitor cells.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2017
    Article
  19. Article
  20. 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

3 authors at 2 institutions in 2 countries.

Michael J CourtneyMolecular Signalling Laboratory, Department of Neurobiology, A. I. Virtanen Institute, University of Eastern Finland Kuopio, Finland ; Turku Centre for Biotechnology, Abo Akademi University and University of Turku Turku, Finland.
Li-Li LiMolecular Signalling Laboratory, Department of Neurobiology, A. I. Virtanen Institute, University of Eastern Finland Kuopio, Finland.
Yvonne Y LaiJack Gill Center for Biomolecular Science, Department Psychological and Brain Sciences, Indiana University Bloomington, IN, USA.
University of Eastern Finland · FIIndiana University Bloomington · US

Funding

Quality Assurance and Quality Control Project Management: Improving Submissions and Study Conduct in the Human Subjects Research Prior Approval ProcessUL1TR002529 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI MOE, SHARON M, WIEHE, SARAH ELIZABETH · 2018 to 2022
$27.2M
Indiana Clinical and Translational Sciences InstituteUL1TR001108 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI DENNE, SCOTT C., SHEKHAR, ANANTHA · 2013 to 2017
$23.3M
Protein-protein interaction inhibitors as novel analgesicsR21DA037673 · NIDA · TRUSTEES OF INDIANA UNIVERSITY · PI HOHMANN, ANDREA GRACE · 2013 to 2014
$429k
Inhibition of nNOS-PSD95 interactions: A novel approach to developing treatmentsR21MH104018 · NIMH · INDIANA UNIVERSITY INDIANAPOLIS · PI SHEKHAR, ANANTHA · 2014 to 2015
$429k
NCATS NIH HHS UL1 TR001108NIDA NIH HHS R21 DA037673NIMH NIH HHS R21 MH104018
6 · The paper itself

Abstract

NMDA receptors (NMDAR) are glutamate-gated calcium channels that play pivotal roles in fundamental aspects of neuronal function. Dysregulated receptor function contributes to many disorders. Recruitment by NMDARs of calcium-dependent enzyme nNOS via PSD95 is seen as a key contributor to neuronal dysfunction. nNOS adaptor protein (NOS1AP), originally described as a competitor of PSD95:nNOS interaction, is regarded an inhibitor of NMDAR-driven nNOS function. In conditions of NMDAR hyperactivity such as excitotoxicity, one expects NOS1AP to be neuroprotective. Conditions of NMDAR hypoactivity, as thought to occur in schizophrenia, might be exacerbated by NOS1AP. Indeed GWAS have implicated NOS1AP and nNOS in schizophrenia. Several studies now indicate NOS1AP can mediate rather than inhibit NMDAR/nNOS-dependent responses, including excitotoxic signaling. Yet the concept of NOS1AP as an inhibitor of nNOS predominates in studies of human disease genetics. Here we review the experimental evidence to evaluate this apparent controversy, consider whether the known functions of NOS1AP might defend neurons against NMDAR dysregulation and highlight specific areas for future investigation to shed light on the functions of this adaptor protein.

Indexed as

excitotoxicitynitric oxideNMDA receptornNOSNOS1APPDZPSD95schizophrenia

Identifiers

PMID25221472
PMCPMC4145862
OpenAlexW2040135097

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.