| Interacting proteins: Q8WTW3 and Q9UP83 |
Pubmed |
SVM Score :0.0 |
| Our results suggest that COG 4 serves as a core component of the complex by interacting directly with COG 1 , COG 2 , COG 5 , and COG 7 . ^^^ |
|
| Interacting proteins: Q8WTW3 and Q9UP83 |
Pubmed |
SVM Score :0.0 |
| We have analyzed the structure and function of COG using Cog 1 or Cog 2 null Chinese hamster ovary cell mutants , fibroblasts from a patient with Cog 7 deficient congenital disorders of glycosylation , and stable Cog 5 deficient HeLa cells generated by RNA interference . ^^^ Although the dilation of some Golgi cisternae in Cog 5 deficient cells resembled that observed in Cog 1 or Cog 2 deficient cells , their global glycosylation defects ( less severe ) and intracellular processing and function of low density lipoprotein receptors ( essentially normal ) differed from Cog 1 and Cog 2 deficient cells . ^^^ Immunoblotting , gel filtration , and immunofluorescence microscopy analyses of the COG deficient cells and cell extracts indicated that 1 ) Cog 2 4 and Cog 5 7 form stable subcomplexes , 2 ) Cog 1 mediates Golgi association of a Cog 2 4 plus Cog 8 subcomplex , 3 ) Cog 8 associates stably with both Cog 5 7 and Cog 1 4 subcomplexes , and thus 4 ) Cog 8 helps assemble the Cog 1 4 and Cog 5 7 subcomplexes into the complete COG complex . ^^^ Only one or two of the seven Cog 1 or Cog 2 dependent Golgi membrane proteins called GEARs are also sensitive to Cog 5 or Cog 7 deficiency , indicating that the COG subunits play distinctive roles in controlling Golgi structure and function . . ^^^ |
|
| Interacting proteins: Q9UP83 and Q8WTW3 |
Pubmed |
SVM Score :0.0 |
| Our results suggest that COG 4 serves as a core component of the complex by interacting directly with COG 1 , COG 2 , COG 5 , and COG 7 . ^^^ |
|
| Interacting proteins: Q9UP83 and Q8WTW3 |
Pubmed |
SVM Score :0.0 |
| We have analyzed the structure and function of COG using Cog 1 or Cog 2 null Chinese hamster ovary cell mutants , fibroblasts from a patient with Cog 7 deficient congenital disorders of glycosylation , and stable Cog 5 deficient HeLa cells generated by RNA interference . ^^^ Although the dilation of some Golgi cisternae in Cog 5 deficient cells resembled that observed in Cog 1 or Cog 2 deficient cells , their global glycosylation defects ( less severe ) and intracellular processing and function of low density lipoprotein receptors ( essentially normal ) differed from Cog 1 and Cog 2 deficient cells . ^^^ Immunoblotting , gel filtration , and immunofluorescence microscopy analyses of the COG deficient cells and cell extracts indicated that 1 ) Cog 2 4 and Cog 5 7 form stable subcomplexes , 2 ) Cog 1 mediates Golgi association of a Cog 2 4 plus Cog 8 subcomplex , 3 ) Cog 8 associates stably with both Cog 5 7 and Cog 1 4 subcomplexes , and thus 4 ) Cog 8 helps assemble the Cog 1 4 and Cog 5 7 subcomplexes into the complete COG complex . ^^^ Only one or two of the seven Cog 1 or Cog 2 dependent Golgi membrane proteins called GEARs are also sensitive to Cog 5 or Cog 7 deficiency , indicating that the COG subunits play distinctive roles in controlling Golgi structure and function . . ^^^ |
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