Evidence map›Paper›PMID 15112102›Full record

ArticleMammalian genome : official journal of the International Mammalian Genome Society2004

Fine mapping of a seizure susceptibility locus on mouse Chromosome 1: nomination of Kcnj10 as a causative gene.

Thomas N Ferraro, Gregory T Golden, George G Smith, James F Martin, Falk W Lohoff, Tracy A Gieringer, Deborah Zamboni, Candice L Schwebel, Danielle M Press, Stephanie O Kratzer and 3 more

Abstract read
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In one paragraph

Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

75 citing papers in PubMed, 149 citations in OpenAlex.

  1. Review
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  4. bioRxiv : the preprint server for biology · 2024
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  5. Review
  6. Review
  7. Article
  8. Review
  9. Pharmacological Approaches to Studying Potassium Channels.Handbook of experimental pharmacology · 2021
    Review
  10. Anti-Kir4.1 Antibodies in Multiple Sclerosis: Specificity and Pathogenicity.International journal of molecular sciences · 2020
    Review
  11. Article
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  14. Review
  15. Neuromodulation of Glial Function During Neurodegeneration.Frontiers in cellular neuroscience · 2020
    Article
  16. Roles of KNeuropharmacology · 2019
    Article
  17. Review
  18. Review
  19. Article
  20. Review

15 more citing papers are in PubMed but not listed here.

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

13 authors at 2 institutions in 1 country.

Thomas N FerraroDepartment of Psychiatry, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. tnf@mail.med.upenn.edu
Gregory T Golden
George G Smith
James F Martin
Falk W Lohoff
Tracy A Gieringer
Deborah Zamboni
Candice L Schwebel
Danielle M Press
Stephanie O Kratzer
Hongyu Zhao
Wade H Berrettini
Russell J Buono
University of Pennsylvania · USYale University · US

Funding

QUANTITATIVE GENETIC STUDY OF SEIZURESR01NS040554 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI FERRARO, THOMAS N · 2000 to 2012
$4.4M
NINDS NIH HHS NS40554
6 · The paper itself

Abstract

Previous quantitative trait loci (QTL) mapping studies document that the distal region of mouse Chromosome (Chr) 1 contains a gene(s) that is in large part responsible for the difference in seizure susceptibility between C57BL/6 (B6) (relatively seizure-resistant) and DBA/2 (D2) (relatively seizure-sensitive) mice. We now confirm this seizure-related QTL ( Szs1) using reciprocal, interval-specific congenic strains and map it to a 6.6-Mb segment between Pbx1 and D1Mit150. Haplotype conservation between strains within this segment suggests that Szs1 may be localized more precisely to a 4.1-Mb critical interval between Fcgr3 and D1Mit150. We compared the coding region sequences of candidate genes between B6 and D2 mice using RT-PCR, amplification from genomic DNA, and database searching and discovered 12 brain-expressed genes with SNPs that predict a protein amino acid variation. Of these, the most compelling seizure susceptibility candidate is Kcnj10. A survey of the Kcnj10 SNP among other inbred mouse strains revealed a significant effect on seizure sensitivity such that most strains possessing a haplotype containing the B6 variant of Kcnj10 have higher seizure thresholds than those strains possessing the D2 variant. The unique role of inward-rectifying potassium ion channels in membrane physiology coupled with previous strong association between ion channel gene mutations and seizure phenotypes puts even greater focus on Kcnj10 in the present model. In summary, we confirmed a seizure-related QTL of large effect on mouse Chr 1 and mapped it to a finely delimited region. The critical interval contains several candidate genes, one of which, Kcnj10, exhibits a potentially important polymorphism with regard to fundamental aspects of seizure susceptibility.

Indexed as

Amino Acid SequenceAnimalsChromosome MappingChromosomes, MammalianCrosses, GeneticDisease SusceptibilityElectroshockFemaleGenotypeMaleMiceMice, Inbred StrainsMicrosatellite RepeatsMolecular Sequence DataPolymorphism, Single NucleotidePotassium Channels, Inwardly RectifyingPotassium Channels, Inwardly RectifyingRNA

Identifiers

PMID15112102
OpenAlexW2072151819

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.