Evidence map›Paper›PMID 23865579›Full record

ArticleTraffic (Copenhagen, Denmark)2013

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

Orly Laufman, Hudson H Freeze, Wanjin Hong, Sima Lev

Abstract read
In one paragraph

Article in Traffic (Copenhagen, Denmark), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Golgi inCOGnito: From vesicle tethering to human disease.Biochimica et biophysica acta. General subjects · 2020
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Bridging the Gap between Glycosylation and Vesicle Traffic.Frontiers in cell and developmental biology · 2016
    Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 3 countries.

Orly LaufmanMolecular Cell Biology Department, Weizmann Institute of Science, Rehovot, 76100, Israel.
Hudson H Freeze
Wanjin Hong
Sima Lev
Weizmann Institute of Science · ILInstitute of Molecular and Cell Biology · SGSanford Burnham Prebys Medical Discovery Institute · US

Funding

Carbohydrate Deficient Glycoprotein Syndromes: Models and TherapyR01DK055615 · NIDDK · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI FREEZE, HUDSON H. · 1999 to 2013
$4.4M
NIDDK NIH HHS R01 DK055615
6 · The paper itself

Abstract

Multiple mutations in different subunits of the tethering complex Conserved Oligomeric Golgi (COG) have been identified as a cause for Congenital Disorders of Glycosylation (CDG) in humans. Yet, the mechanisms by which COG mutations induce the pleiotropic CDG defects have not been fully defined. By detailed analysis of Cog8 deficiency in either HeLa cells or CDG-derived fibroblasts, we show that Cog8 is required for the assembly of both the COG complex and the Golgi Stx5-GS28-Ykt6-GS15 and Stx6-Stx16-Vti1a-VAMP4 SNARE complexes. The assembly of these SNARE complexes is also impaired in cells derived from a Cog7-deficient CDG patient. Likewise, the integrity of the COG complex is also impaired in Cog1-, Cog4- and Cog6-depleted cells. Significantly, deficiency of Cog1, Cog4, Cog6 or Cog8 distinctly influences the production of COG subcomplexes and their Golgi targeting. These results shed light on the structural organization of the COG complex and its subcellular localization, and suggest that its integrity is required for both tethering of transport vesicles to the Golgi apparatus and the assembly of Golgi SNARE complexes. We propose that these two key functions are generally and mechanistically impaired in COG-associated CDG patients, thereby exerting severe pleiotropic defects.

Indexed as

Adaptor Proteins, Vesicular TransportAnimalsCell LineCell Line, TumorCHO CellsCongenital Disorders of GlycosylationCricetulusFibroblastsGlycosylationGolgi ApparatusHEK293 CellsHeLa CellsHumansMutationProtein SubunitsProtein TransportAdaptor Proteins, Vesicular TransportCOG8 protein, humanProtein SubunitsSNARE ProteinsCDGCOG complexGolgiSNAREtethering

Identifiers

PMID23865579
PMCPMC4084554
OpenAlexW1930536419

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.