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

Null mutations in Drosophila N-acetylglucosaminyltransferase I produce defects in locomotion and a reduced life span.

The Journal of biological chemistry - 5 May 2006

Sarkar Mohan, Leventis Peter A, Silvescu Cristina I, Reinhold Vernon N, Schachter Harry, Boulianne Gabrielle L

Abstract excerpt

UDP-GlcNAc:alpha3-D-mannoside beta1,2-N-acetylglucosaminyltransferase I (encoded by Mgat1) controls the synthesis of hybrid, complex, and paucimannose N-glycans. Mice make hybrid and complex N-glycans but little or no paucimannose N-glycans. In contrast, Drosophila melanogaster and Caenorhabditis elegans make paucimannose N-glycans but little or no hybrid or complex N-glycans. To determine the functional...

Read the complete abstract on PubMed

Topics

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

Share to Animals, Genetically Modified
Share to Caenorhabditis elegans

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Carbohydrate Conformation

Share to Drosophila melanogaster

Share to Green Fluorescent Proteins

Share to Mass Spectrometry

Share to N-Acetylglucosaminyltransferases

Share to Polysaccharides

Source

Identifiers

PMID: 16522637
DOI: 10.1074/jbc.M512769200

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

Null mutations in Drosophila N-acetylglucosaminyltransferase I produce defects in locomotion and a reduced life span.PMID 16522637Read ↗

Neuronal expression of Mgat1 rescues the shortened life span of Drosophila Mgat11 null mutants and increases life span.Semantic proximity Read ↗

Functional analysis of Drosophila beta1,4-N-acetlygalactosaminyltransferases.Semantic proximity Read ↗

Mgat1-dependent N-glycans are essential for the normal development of both vertebrate and invertebrate metazoans.Semantic proximity Read ↗

Requirement for a core 1 galactosyltransferase in the Drosophila nervous system.Semantic proximity Read ↗

Mutant analysis reveals an alternative pathway for N-linked glycosylation in Drosophila melanogaster.Semantic proximity Read ↗

Ablation of N-acetylglucosaminyltransferases in Caenorhabditis induces expression of unusual intersected and bisected N-glycans.Semantic proximity Read ↗

Functional analysis of glycosylation using Drosophila melanogaster.Semantic proximity Read ↗

Drosophila GFAT1 and GFAT2 enzymes encode obligate developmental functions.Semantic proximity Read ↗

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

Caenorhabditis elegans triple null mutant lacking UDP-N-acetyl-D-glucosamine:alpha-3-D-mannoside beta1,2-N-acetylglucosaminyltransferase I.Semantic proximity Read ↗

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

The directed migration of gonadal distal tip cells in Caenorhabditis elegans requires NGAT-1, a ß1,4-N-acetylgalactosaminyltransferase enzyme.Semantic proximity Read ↗

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