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COG7  -  component of oligomeric golgi complex 7

Homo sapiens

Synonyms: COG complex subunit 7, Component of oligomeric Golgi complex 7, Conserved oligomeric Golgi complex subunit 7, UNQ3082/PRO10013
 
 
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High impact information on COG7

  • All of these abnormalities were normalized in COG7-corrected patient fibroblasts [1].
  • Recently, we reported that two siblings presenting with the clinical syndrome congenital disorders of glycosylation (CDG) have mutations in the gene encoding Cog7p, a member of the conserved oligomeric Golgi (COG) complex [1].
  • Genetic analysis of the subunit organization and function of the conserved oligomeric golgi (COG) complex: studies of COG5- and COG7-deficient mammalian cells [2].
  • COG7 KD and double COG3/COG7 KD caused similar defects with respect to both Golgi traffic and glycosylation, suggesting that the entire COG complex orchestrates recycling of medial-Golgi-resident proteins [3].
  • In a consecutive study a defect in the conserved oligomeric Golgi complex was established at the level of subunit COG-7, leading to disruption of multiple glycosylation functions of the Golgi [4].

References

  1. COG-7-deficient Human Fibroblasts Exhibit Altered Recycling of Golgi Proteins. Steet, R., Kornfeld, S. Mol. Biol. Cell (2006) [Pubmed]
  2. Genetic analysis of the subunit organization and function of the conserved oligomeric golgi (COG) complex: studies of COG5- and COG7-deficient mammalian cells. Oka, T., Vasile, E., Penman, M., Novina, C.D., Dykxhoorn, D.M., Ungar, D., Hughson, F.M., Krieger, M. J. Biol. Chem. (2005) [Pubmed]
  3. COG complex-mediated recycling of Golgi glycosyltransferases is essential for normal protein glycosylation. Shestakova, A., Zolov, S., Lupashin, V. Traffic (2006) [Pubmed]
  4. Clinical and biochemical presentation of siblings with COG-7 deficiency, a lethal multiple O- and N-glycosylation disorder. Spaapen, L.J., Bakker, J.A., van der Meer, S.B., Sijstermans, H.J., Steet, R.A., Wevers, R.A., Jaeken, J. J. Inherit. Metab. Dis. (2005) [Pubmed]
 
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