Evidence map›Paper›PMID 24095980›Full record

ArticleExperimental neurology2013

Deletion in the N-terminal half of olfactomedin 1 modifies its interaction with synaptic proteins and causes brain dystrophy and abnormal behavior in mice.

Naoki Nakaya, Afia Sultana, Jeeva Munasinghe, Aiwu Cheng, Mark P Mattson, Stanislav I Tomarev

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

24 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  7. Obesity wars: may the smell be with you.American journal of physiology. Endocrinology and metabolism · 2023
    Review
  8. Human Astrocytes Exhibit Tumor Microenvironment-, Age-, and Sex-Related Transcriptomic Signatures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  9. Article
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  12. Review
  13. Article
  14. Review
  15. Microglia-Specific Expression ofFrontiers in immunology · 2018
    Article
  16. Article
  17. Myocilin Regulates Metalloprotease 2 Activity Through Interaction With TIMP3.Investigative ophthalmology & visual science · 2017
    Article
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 1 country.

Naoki NakayaGanglion Cell Biology Section, Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, NIH, Bethesda, MD 20892, USA. Electronic address: nakayan@nei.nih.gov.
Afia Sultana
Jeeva Munasinghe
Aiwu Cheng
Mark P Mattson
Stanislav I Tomarev
National Eye Institute · USNational Institute on Aging · USNational Institute of Neurological Disorders and Stroke · US

Funding

Molecular Genetics Of Early Eye DevelopmentZIAEY000311 · NEI · NATIONAL EYE INSTITUTE · PI TOMAREV, STANISLAV I · 2009 to 2025
$10.6M
MOLECULAR GENETICS OF EARLY EYE DEVELOPMENTZ01EY000311 · NEI · NATIONAL EYE INSTITUTE · PI TOMAREV, STANISLAV I · 1996 to 2008
$941k
Intramural NIH HHS Z01 EY000311
6 · The paper itself

Abstract

Olfactomedin 1 (Olfm1) is a secreted glycoprotein that is preferentially expressed in neuronal tissues. Here we show that deletion of exons 4 and 5 from the Olfm1 gene, which encodes a 52 amino acid long region in the N-terminal part of the protein, increased neonatal death and reduced body weight of surviving homozygous mice. Magnetic resonance imaging analyses revealed reduced brain volume and attenuated size of white matter tracts such as the anterior commissure, corpus callosum, and optic nerve. Adult Olfm1 mutant mice demonstrated abnormal behavior in several tests including reduced marble digging, elevated plus maze test, nesting activity and latency on balance beam tests as compared with their wild-type littermates. The olfactory system was both structurally and functionally disturbed by the mutation in the Olfm1 gene as shown by functional magnetic resonance imaging analysis and a smell test. Deficiencies of the olfactory system may contribute to the neonatal death and loss of body weight of Olfm1 mutant. Shotgun proteomics revealed 59 candidate proteins that co-precipitated with wild-type or mutant Olfm1 proteins in postnatal day 1 brain. Olfm1-binding targets included GluR2, Cav2.1, teneurin-4 and Kidins220. Modified interaction of Olfm1 with binding targets led to an increase in intracellular Ca(2+) concentration and activation of ERK1/2, MEK1 and CaMKII in the hippocampus and olfactory bulb of Olfm1 mutant mice compared with their wild-type littermates. Excessive activation of the CaMKII and Ras-ERK pathways in the Olfm1 mutant olfactory bulb and hippocampus by elevated intracellular calcium may contribute to the abnormal behavior and olfactory activity of Olfm1 mutant mice.

Indexed as

Amino Acid SequenceAnimalsBehavior, AnimalBlotting, WesternBrainExonsExtracellular Matrix ProteinsFemaleGlycoproteinsImmunoprecipitationMagnetic Resonance ImagingMaleMiceMice, Mutant StrainsMolecular Sequence DataProteomicsExtracellular Matrix ProteinsGlycoproteinsolfactomedinAMPA receptorAnxiety behaviorCell signalingMagnetic resonance imagingMouseMRINeurobiologyOlfactomedin 1Olfactory defectsOlfm1Olfm1 knockoutOlfm1-KOProteomicsQ-PCRQuantitative RT-PCR

Identifiers

PMID24095980
PMCPMC3875227
OpenAlexW2052345184

What OpenQuestion holds

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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.