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

Genome-wide gene expression profiling of the Angelman syndrome mice with Ube3a mutation.

European journal of human genetics : EJHG - 1 Nov 2010

Low Daren, Chen Ken-Shiung

Abstract excerpt

Angelman syndrome (AS) is a human neurological disorder caused by lack of maternal UBE3A expression in the brain. UBE3A is known to function as both an ubiquitin-protein ligase (E3) and a coactivator for steroid receptors. Many ubiquitin targets, as well as interacting partners, of UBE3A have bee...

Read the complete abstract on PubMed

Topics

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

Share to Angelman Syndrome
Share to Cerebellum
Share to Gene Regulatory Networks

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Nuclear Receptor Subfamily 4, Group A, Member 2

Share to Oligonucleotide Array Sequence Analysis

Share to Receptor, Melanocortin, Type 1

Share to RNA Interference

Share to Ubiquitin-Protein Ligases

Source

Open in PubMed Open full text

Identifiers

PMID: 20571502
DOI: 10.1038/ejhg.2010.95
PMCID: PMC2987484

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-20571502-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Genome-wide gene expression profiling of the Angelman syndrome mice with Ube3a mutation.PMID 20571502Read ↗

Angelman syndrome: insights into genomic imprinting and neurodevelopmental phenotypes.Semantic proximity Read ↗

Angelman Syndrome causing UBE3A ligase displays predominantly synaptic ubiquitination activity in the mouse brainSemantic proximity Read ↗

Deleting a UBE3A substrate rescues impaired hippocampal physiology and learning in Angelman syndrome miceSemantic proximity Read ↗

Imprinting effects of UBE3A loss on synaptic gene networks and Wnt signaling pathwaysSemantic proximity Read ↗

Imprinting effects of UBE3A loss on synaptic gene networks and Wnt signaling pathwaysSemantic proximity Read ↗

Angelman Syndrome: From Mouse Models to Therapy.Semantic proximity Read ↗

Angelman Syndrome.Semantic proximity Read ↗

Dysregulation of neuronal activity-dependent immediate early genes in a mouse model of Angelman syndromeSemantic proximity Read ↗

Toward a Broader View of Ube3a in a Mouse Model of Angelman Syndrome: Expression in Brain, Spinal Cord, Sciatic Nerve and Glial Cells.Semantic proximity Read ↗

Emerging Gene and Small Molecule Therapies for the Neurodevelopmental Disorder Angelman SyndromeSemantic proximity Read ↗

Angelman syndrome: how many genes to remain silent?Semantic proximity Read ↗

A novel UBE3A sequence variant identified in eight related individuals with neurodevelopmental delay, results in a phenotype which does not match the clinical criteria of Angelman syndrome.Semantic proximity Read ↗

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