Evidence map›Paper›PMID 19666602›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Mutation I810N in the alpha3 isoform of Na+,K+-ATPase causes impairments in the sodium pump and hyperexcitability in the CNS.

Steven J Clapcote, Steven Duffy, Gang Xie, Greer Kirshenbaum, Allison R Bechard, Vivien Rodacker Schack, Janne Petersen, Laleh Sinai, Bechara J Saab, Jason P Lerch and 7 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

88 citing papers in PubMed, 151 citations in OpenAlex.

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  14. Sensational site: the sodium pump ouabain-binding site and its ligands.American journal of physiology. Cell physiology · 2024
    Review
  15. International journal of molecular sciences · 2023
    Article
  16. Article
  17. NaBiomedicines · 2023
    Review
  18. The role ofFrontiers in cellular neuroscience · 2023
    Review
  19. NaInternational journal of molecular sciences · 2022
    Article
  20. The role of NaCNS neuroscience & therapeutics · 2022
    Review

28 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

17 authors at 6 institutions in 3 countries.

Steven J ClapcoteSamuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, ON, Canada M5G 1X5. s.j.clapcote@leeds.ac.uk
Steven Duffy
Gang Xie
Greer Kirshenbaum
Allison R Bechard
Vivien Rodacker Schack
Janne Petersen
Laleh Sinai
Bechara J Saab
Jason P Lerch
Berge A Minassian
Cameron A Ackerley
John G Sled
Miguel A Cortez
Jeffrey T Henderson
Bente Vilsen
John C Roder
University of Toronto · CADanish National Research Foundation · DKHospital for Sick Children · CALunenfeld-Tanenbaum Research Institute · CAMount Sinai Hospital · CAUniversity of Leeds · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In a mouse mutagenesis screen, we isolated a mutant, Myshkin (Myk), with autosomal dominant complex partial and secondarily generalized seizures, a greatly reduced threshold for hippocampal seizures in vitro, posttetanic hyperexcitability of the CA3-CA1 hippocampal pathway, and neuronal degeneration in the hippocampus. Positional cloning and functional analysis revealed that Myk/+ mice carry a mutation (I810N) which renders the normally expressed Na(+),K(+)-ATPase alpha3 isoform inactive. Total Na(+),K(+)-ATPase activity was reduced by 42% in Myk/+ brain. The epilepsy in Myk/+ mice and in vitro hyperexcitability could be prevented by delivery of additional copies of wild-type Na(+),K(+)-ATPase alpha3 by transgenesis, which also rescued Na(+),K(+)-ATPase activity. Our findings reveal the functional significance of the Na(+),K(+)-ATPase alpha3 isoform in the control of epileptiform activity and seizure behavior.

Indexed as

MutationAnimalsBase SequenceCentral Nervous SystemChlorocebus aethiopsCOS CellsHippocampusMaleMiceMice, Inbred C57BLMolecular Sequence DataSeizuresSequence Homology, Nucleic AcidSodium-Potassium-Exchanging ATPaseAtp1a3 protein, mouseSodium-Potassium-Exchanging ATPase

Identifiers

PMID19666602
PMCPMC2729024
OpenAlexW2051736421

What OpenQuestion 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 OpenQuestion graph.