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COG6 Cog6p

COD2, Cog6p, SEC37, COG6
This gene encodes a subunit of the conserved oligomeric Golgi complex that is required for maintaining normal structure and activity of the Golgi apparatus. The encoded protein is organized with conserved oligomeric Golgi complex components 5, 7 and 8 into a sub-complex referred to as lobe B. Alternative splicing results in multiple transcript variants.[provided by RefSeq, Feb 2009] (from NCBI)
Top mentioned proteins: COG4, IL12B, MHC, CAN, EB1
Papers on COD2
Key features and clinical variability of COG6-CDG.
Kornak et al., Leuven, Belgium. In Mol Genet Metab, Nov 2015
So far, 3 families with a total of 10 individuals with biallelic COG6 mutations have been described, showing a broad clinical spectrum.
High-density genotyping of immune loci in Koreans and Europeans identifies eight new rheumatoid arthritis risk loci.
Bae et al., Cambridge, United States. In Ann Rheum Dis, Mar 2015
RESULTS: We identified eight new rheumatoid arthritis susceptibility loci (TNFSF4, LBH, EOMES, ETS1-FLI1, COG6, RAD51B, UBASH3A and SYNGR1) that passed a genome-wide significance threshold (p<5×10(-8)), with evidence for three independent risk alleles at 1q25/TNFSF4.
Genome-wide meta-analysis identifies multiple novel associations and ethnic heterogeneity of psoriasis susceptibility.
Liu et al., Hefei, China. In Nat Commun, 2014
We identify four novel associations at LOC144817, COG6, RUNX1 and TP63, as well as three novel secondary associations within IFIH1 and IL12B.
Investigating the genetic association of HCP5, SPATA2, TNIP1, TNFAIP3 and COG6 with psoriasis in Chinese population.
Wu et al., Kunming, China. In Int J Immunogenet, 2014
The genes HLA complex P5 (HCP5), spermatogenesis associated 2 (SPATA2), tumour necrosis factor alpha-induced protein 3 (TNFAIP3), TNFAIP3-interacting protein 1 (TNIP1) and the component of oligomeric Golgi complex 6 (COG6) were reported to be associated with psoriasis in western populations by genome-wide association studies.
Target silencing of components of the conserved oligomeric Golgi complex impairs HIV-1 replication.
Dykxhoorn et al., Miami, United States. In Virus Res, 2014
The targeted silencing of components of lobe B of the COG complex, namely COG5, COG6, COG7 and COG8, inhibited HIV-1 replication.
Polymorphism in miRNA-1 target site and circulating miRNA-1 phenotype are associated with the decreased risk and prognosis of coronary artery disease.
Wei et al., Nanjing, China. In Int J Clin Exp Pathol, 2013
A case-control study was designed to assess the relationship between miRNA-1 target site rs9548934C→T polymorphism in target gene (Component of Oligomeric Golgi Complex 6, COG6) and risk of coronary artery disease (CAD) in 1013 patients and 610 normal controls.
A novel syndrome of hypohidrosis and intellectual disability is linked to COG6 deficiency.
Alkuraya et al., Riyadh, Saudi Arabia. In J Med Genet, 2013
variant in COG6 that largely replaces the consensus acceptor site, resulting in pronounced reduction of the normal transcript and consequent deficiency of COG6 protein.
COG6 interacts with a subset of the Golgi SNAREs and is important for the Golgi complex integrity.
Lupashin et al., Little Rock, United States. In Traffic, 2013
Using yeast two-hybrid and co-immunoprecipitation approaches, we show that the COG6 subunit of the COG complex is capable of interacting with a subset of Golgi SNAREs, namely STX5, STX6, GS27 and SNAP29.
Gamma-tocotrienol modulated gene expression in senescent human diploid fibroblasts as revealed by microarray analysis.
Ngah et al., Kuala Lumpur, Malaysia. In Oxid Med Cell Longev, 2012
Amongst the genes were IRAK3, SelS, HSPA5, HERPUD1, DNAJB9, SEPR1, C18orf55, ARF4, RINT1, NXT1, CADPS2, COG6, and GLRX5.
Risk variants for psoriasis vulgaris in a large case-control collection and association with clinical subphenotypes.
Marsal et al., Barcelona, Spain. In Hum Mol Genet, 2012
We provide the first independent replication for COG6 (P = 0.00079) and SERPINB8 (P = 0.048) loci with PsV.
[Association study on the microRNA-1 target gene polymorphism and the risk of premature coronary artery disease].
Wang et al., Nanjing, China. In Zhonghua Xin Xue Guan Bing Za Zhi, 2012
OBJECTIVE: To investigate the association between the genetic variant of miRNA-1 target gene COG6 rs9548934 C→T and the risk of premature coronary artery disease (pCAD).
Conserved oligomeric Golgi complex specifically regulates the maintenance of Golgi glycosylation machinery.
Lupashin et al., Little Rock, United States. In Glycobiology, 2011
The lobe B COG subcomplex subunits COG6 and COG8 were localized on trafficking intermediates that carry Golgi glycosyltransferases, indicating that the COG complex is directly involved in trafficking and maintenance of Golgi glycosylation machinery.
Deficiency of Subunit 6 of the Conserved Oligomeric Golgi Complex (COG6-CDG): Second Patient, Different Phenotype.
Goyens et al., Brussels, Belgium. In Jimd Rep, 2011
We describe a 27-month-old girl with COG6 deficiency.
The COG complex interacts directly with Syntaxin 6 and positively regulates endosome-to-TGN retrograde transport.
Lev et al., Israel. In J Cell Biol, 2011
COG directly and positively regulates endosome-to-TGN retrograde transport by specific and direct interaction with the t-SNARE Stx6 via its Cog6 subunit.
The susceptibility loci juvenile idiopathic arthritis shares with other autoimmune diseases extend to PTPN2, COG6, and ANGPT1.
Langefeld et al., Cincinnati, United States. In Arthritis Rheum, 2010
P = 2.59 × 10(-5) ]), COG6 (rs7993214 [OR = 0.76, P = 1.10 × 10(-5) ]), and ANGPT1 (rs1010824 [OR = 0.79, P = 2.91 × 10(-4) ]).
Fatal outcome due to deficiency of subunit 6 of the conserved oligomeric Golgi complex leading to a new type of congenital disorders of glycosylation.
Körner et al., Heidelberg, Germany. In Hum Mol Genet, 2010
Deficiency of subunit 6 of the conserved oligomeric Golgi (COG6) complex causes a new combined N- and O-glycosylation deficiency of the congenital disorders of glycosylation, designated as CDG-IIL (COG6-CDG).
COG8 deficiency causes new congenital disorder of glycosylation type IIh.
Freeze et al., Los Angeles, United States. In Hum Mol Genet, 2007
This paper reports a new congenital disorder caused by mutations in the human COG8 gene and describes the affect this mutation has on the other COG components.
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