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

COG7 deficiency in Drosophila generates multifaceted developmental, behavioral and protein glycosylation phenotypes.

Journal of cell science - 1 Nov 2017

Frappaolo Anna, Sechi Stefano, Kumagai Tadahiro, Robinson Sarah, Fraschini Roberta, Karimpour-Ghahnavieh Angela, Belloni Giorgio, Piergentili Roberto, Tiemeyer Katherine H, Tiemeyer Michael, Giansanti Maria Grazia

Abstract excerpt

Congenital disorders of glycosylation (CDG) comprise a family of human multisystemic diseases caused by recessive mutations in genes required for protein N-glycosylation. More than 100 distinct forms of CDGs have been identified and most of them cause severe neurological impairment. The Conserved Oligomeric Golgi (COG) complex mediates tethering of vesicles carrying glycosylation enzymes across the Golgi...

Read the complete abstract on PubMed

Topics

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

Share to Congenital Disorders of Glycosylation
Share to Gait Disorders, Neurologic

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Golgi Apparatus

Share to Mannose

Share to Neuromuscular Junction

Share to Oncogene Proteins

Share to Polysaccharides

Share to rab GTP-Binding Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 28883096
DOI: 10.1242/jcs.209049
PMCID: PMC5702061

Genes

COG7
COG1
COG2
COG4
COG8

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

COG7 deficiency in Drosophila generates multifaceted developmental, behavioral and protein glycosylation phenotypes.PMID 28883096Read ↗

COG Complex in Golgi Trafficking and Glycosylation.Semantic proximity Read ↗

Synaptic roles for phosphomannomutase type 2 in a new Drosophila congenital disorder of glycosylation disease modelSemantic proximity Read ↗

Mutations in Cog7 affect Golgi structure, meiotic cytokinesis and sperm development during Drosophila spermatogenesis.Semantic proximity Read ↗

Golgi inCOGnito: From vesicle tethering to human disease.Semantic proximity Read ↗

More than just sugars: Conserved oligomeric Golgi complex deficiency causes glycosylation-independent cellular defects.Semantic proximity Read ↗

Deficiency of the Cog8 subunit in normal and CDG-derived cells impairs the assembly of the COG and Golgi SNARE complexes.Semantic proximity Read ↗

Neuromuscular Defects in a Drosophila Model of the Congenital Disorder of Glycosylation SLC35A2-CDG.Semantic proximity Read ↗

Mutation of the COG complex subunit gene COG7 causes a lethal congenital disorder.Semantic proximity Read ↗

Deficiencies in subunits of the Conserved Oligomeric Golgi (COG) complex define a novel group of Congenital Disorders of Glycosylation.Semantic proximity Read ↗

GOLGA2, encoding a master regulator of golgi apparatus, is mutated in a patient with a neuromuscular disorder.Semantic proximity Read ↗

Biallelic missense variants in COG3 cause a congenital disorder of glycosylation with impairment of retrograde vesicular trafficking.Semantic proximity Read ↗

Mutations in COG2 encoding a subunit of the conserved oligomeric golgi complex cause a congenital disorder of glycosylation.Semantic proximity Read ↗

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