Evidence map›Paper›PMID 19150498›Full record

ArticleNeurobiology of disease2009

Absence epilepsy in apathetic, a spontaneous mutant mouse lacking the h channel subunit, HCN2.

Wendy K Chung, Minyoung Shin, Thomas C Jaramillo, Rudolph L Leibel, Charles A LeDuc, Stuart G Fischer, Efthia Tzilianos, Ayman A Gheith, Alan S Lewis, Dane M Chetkovich

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

45 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Heterozygous GABAEpilepsia · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Cardiac and neuronal HCN channelopathies.Pflugers Archiv : European journal of physiology · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. A Loss-of-FunctionFrontiers in molecular neuroscience · 2018
    Article
  18. 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

10 authors at 2 institutions in 1 country.

Wendy K ChungDivision of Molecular Genetics and the Naomi Berrie Diabetes Center, Columbia University Medical College, Russell Berrie Medical Science Pavilion, Room 620, 1150 St. Nicholas Avenue, New York, NY 10032, USA.
Minyoung Shin
Thomas C Jaramillo
Rudolph L Leibel
Charles A LeDuc
Stuart G Fischer
Efthia Tzilianos
Ayman A Gheith
Alan S Lewis
Dane M Chetkovich
Columbia University · USNorthwestern University · US

Funding

The molecular genetic analysis of human obesityR01DK052431 · NIDDK · ROCKEFELLER UNIVERSITY · PI CHUNG, WENDY K, LEIBEL, RUDOLPH L · 1996 to 2020
$11.6M
CORE--LABORATORYP30HD034611 · NICHD · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LI, SUZANNE · 1998 to 2002
$969k
Role of HCN channels in epilepsyR21NS052595 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CHETKOVICH, DANE M · 2006 to 2007
$363k
NICHD NIH HHS P30 HD34611NIDDK NIH HHS R01 DK052431NINDS NIH HHS R21 NS052595
6 · The paper itself

Abstract

Analysis of naturally occurring mutations that cause seizures in rodents has advanced understanding of the molecular mechanisms underlying epilepsy. Abnormalities of I(h) and h channel expression have been found in many animal models of absence epilepsy. We characterized a novel spontaneous mutant mouse, apathetic (ap/ap), and identified the ap mutation as a 4 base pair insertion within the coding region of Hcn2, the gene encoding the h channel subunit 2 (HCN2). We demonstrated that Hcn2(ap) mRNA is reduced by 90% compared to wild type, and the predicted truncated HCN2(ap) protein is absent from the brain tissue of mice carrying the ap allele. ap/ap mice exhibited ataxia, generalized spike-wave absence seizures, and rare generalized tonic-clonic seizures. ap/+ mice had a normal gait, occasional absence seizures and an increased severity of chemoconvulsant-induced seizures. These findings help elucidate basic mechanisms of absence epilepsy and suggest HCN2 may be a target for therapeutic intervention.

Indexed as

Amino Acid SequenceAnimalsAtaxiaBase SequenceBody SizeBrainChlorocebus aethiopsConvulsantsCOS CellsCyclic Nucleotide-Gated Cation ChannelsEpilepsy, AbsenceFemaleFrameshift MutationGaitHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsIon ChannelsConvulsantsCyclic Nucleotide-Gated Cation ChannelsHcn2 protein, mouseHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsIon ChannelsPotassium ChannelsRNA, Messenger

Identifiers

PMID19150498
PMCPMC2643333
OpenAlexW1991176458

What OpenQuestion holds

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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.