Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Unraveling genetic modifiers in the gria4 mouse model of absence epilepsy.

PLoS genetics - 1 Jul 2014

Frankel Wayne N, Mahaffey Connie L, McGarr Tracy C, Beyer Barbara J, Letts Verity A

Abstract excerpt

Absence epilepsy (AE) is a common type of genetic generalized epilepsy (GGE), particularly in children. AE and GGE are complex genetic diseases with few causal variants identified to date. Gria4 deficient mice provide a model of AE, one for which the common laboratory inbred strain C3H/HeJ (HeJ) harbors a natural IAP retrotransposon insertion in Gria4 that reduces its expression 8-fold. Between C3H and...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Chromosome Mapping
Share to Disease Models, Animal
Share to Epilepsy, Absence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Neoplasm Proteins

Share to Receptors, AMPA

Share to Retroelements

Share to Seizures

Source

Open in PubMed Open full text

Identifiers

PMID: 25010494
DOI: 10.1371/journal.pgen.1004454
PMCID: PMC4091709

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Unraveling genetic modifiers in the gria4 mouse model of absence epilepsy.PMID 25010494Read ↗

Network-based analysis predicts interacting genetic modifiers from a meta-mapping study of spike-wave discharge in mice.Semantic proximity Read ↗

Genetic complexity of absence seizures in substrains of C3H mice.Semantic proximity Read ↗

A genetic interaction network model of a complex neurological disease.Semantic proximity Read ↗

Genetics of complex neurological disease: challenges and opportunities for modeling epilepsy in mice and rats.Semantic proximity Read ↗

Fine Mapping of a Dravet Syndrome Modifier Locus on Mouse Chromosome 5 and Candidate Gene Analysis by RNA-Seq.Semantic proximity Read ↗

Fine mapping and candidate gene analysis of a dravet syndrome modifier locus on mouse chromosome 11.Semantic proximity Read ↗

Mapping genetic modifiers of survival in a mouse model of Dravet syndromeSemantic proximity Read ↗

Investigation of GRIN2A in common epilepsy phenotypes.Semantic proximity Read ↗

Complex seizure disorder caused by Brunol4 deficiency in mice.Semantic proximity Read ↗

Detecting genes in new and old mouse models for epilepsy: a prospectus through the magnifying glass.Semantic proximity Read ↗

A locus on mouse Ch10 influences susceptibility to limbic seizure severity: fine mapping and in silico candidate gene analysis.Semantic proximity Read ↗

Gene therapies alleviate absence epilepsy associated with <i>Scn2a</i> deficiency in DBA/2J miceSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.