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

O-GlcNAc cycling mutants modulate proteotoxicity in Caenorhabditis elegans models of human neurodegenerative diseases.

Proceedings of the National Academy of Sciences of the United States of America - 23 Oct 2012

Wang Peng, Lazarus Brooke D, Forsythe Michele E, Love Dona C, Krause Michael W, Hanover John A

Abstract excerpt

O-GlcNAcylation is an abundant posttranslational modification in the brain implicated in human neurodegenerative diseases. We have exploited viable null alleles of the enzymes of O-GlcNAc cycling to examine the role of O-GlcNAcylation in well-characterized Caenorhabditis elegans models of neurodegenerative proteotoxicity. O-GlcNAc cycling dramatically modulated the severity of the phenotype in transgenic models...

Read the complete abstract on PubMed

Topics

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

Share to Acetylglucosamine
Share to Alleles

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Caenorhabditis elegans

Share to Disease Models, Animal

Share to Mutation

Share to Neurodegenerative Diseases

Share to Proteolysis

Source

Open in PubMed Open full text

Identifiers

PMID: 22988095
DOI: 10.1073/pnas.1205748109
PMCID: PMC3491483

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

O-GlcNAc cycling mutants modulate proteotoxicity in Caenorhabditis elegans models of human neurodegenerative diseases.PMID 22988095Read ↗

Proteome-based investigation of O-GlcNAcylation in a <i>C. elegans</i> model of Ageing and Alzheimer’s disease: Functional Support for Earlier Hypothesis-Generating FindingsSemantic proximity Read ↗

O-GlcNAc cycling modulates neurodegeneration.Semantic proximity Read ↗

Caenorhabditis elegans ortholog of a diabetes susceptibility locus: oga-1 (O-GlcNAcase) knockout impacts O-GlcNAc cycling, metabolism, and dauer.Semantic proximity Read ↗

Intellectual disability-associated disruption of O-GlcNAcylation impairs neuronal development and cognitive function in <i>Drosophila</i>Semantic proximity Read ↗

Intracellular protein glycosylation modulates insulin mediated lifespan in C.elegans.Semantic proximity Read ↗

Regulation of Dauer formation by O-GlcNAcylation in Caenorhabditis elegans.Semantic proximity Read ↗

Neurodegenerative disorders: insights from the nematode Caenorhabditis elegans.Semantic proximity Read ↗

Caenorhabditis elegans Models to Investigate the Mechanisms Underlying Tau Toxicity in TauopathiesSemantic proximity Read ↗

Drosophila O-GlcNAcase Mutants Reveal an Expanded Glycoproteome and Novel Growth and Longevity Phenotypes.Semantic proximity Read ↗

Mechanisms of aging-related proteinopathies in Caenorhabditis elegansSemantic proximity Read ↗

Rescuable sleep and synaptogenesis phenotypes in a Drosophila model of O-GlcNAc transferase intellectual disability.Semantic proximity Read ↗

Genetic rescue of pathogenic O-GlcNAc dyshomeostasis associated with microcephaly and motor deficitsSemantic proximity Read ↗

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