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

The phosphatase activity of laforin is dispensable to rescue Epm2a-/- mice from Lafora disease.

Brain : a journal of neurology - 1 Mar 2014

Gayarre Javier, Duran-Trío Lara, Criado Garcia Olga, Aguado Carmen, Juana-López Lucia, Crespo Inmaculada, Knecht Erwin, Bovolenta Paola, Rodríguez de Córdoba Santiago

Abstract excerpt

Lafora progressive myoclonus epilepsy (Lafora disease) is a fatal autosomal recessive neurodegenerative disorder characterized by the presence of glycogen-like intracellular inclusions called Lafora bodies. The vast majority of patients carry mutations in either the EPM2A or EPM2B genes, encoding...

Read the complete abstract on PubMed

Topics

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

Share to Autophagy
Share to Dual-Specificity Phosphatases
Share to Lafora Disease

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mice, Inbred C57BL

Share to Mice, Knockout

Share to Mice, Transgenic

Share to Phosphorylation

Share to Protein Tyrosine Phosphatases, Non-Receptor

Source

Identifiers

PMID: 24430976
DOI: 10.1093/brain/awt353

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-24430976-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The phosphatase activity of laforin is dispensable to rescue Epm2a-/- mice from Lafora disease.PMID 24430976Read ↗

Increased Endoplasmic Reticulum Stress and Decreased Proteasomal Function in Lafora Disease Models Lacking the Phosphatase LaforinSemantic proximity Read ↗

Lafora bodies and neurological defects in malin-deficient mice correlate with impaired autophagySemantic proximity Read ↗

Impaired malin expression and interaction with partner proteins in Lafora diseaseSemantic proximity Read ↗

Deciphering the role of malin in the lafora progressive myoclonus epilepsySemantic proximity Read ↗

Mechanism suppressing glycogen synthesis in neurons and its demise in progressive myoclonus epilepsy.Semantic proximity Read ↗

Pathogenesis of Lafora Disease: Transition of Soluble Glycogen to Insoluble PolyglucosanSemantic proximity Read ↗

Relationship between glycogen accumulation and the laforin dual specificity phosphatase.Semantic proximity Read ↗

Lafora disease: from genotype to phenotype.Semantic proximity Read ↗

Laforin is a glycogen phosphatase, deficiency of which leads to elevated phosphorylation of glycogen in vivo.Semantic proximity Read ↗

Laforin targets malin to glycogen in Lafora progressive myoclonus epilepsySemantic proximity Read ↗

Lafora diseaseSemantic proximity Read ↗

Lafora progressive myoclonus epilepsy: Disease mechanism and therapeutic attempts.Semantic proximity Read ↗

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