ArticleThe Journal of cell biology1994
LDLC encodes a brefeldin A-sensitive, peripheral Golgi protein required for normal Golgi function.
Article in The Journal of cell biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 60 citations in OpenAlex.
- COG Complex in Golgi Trafficking and Glycosylation.Sub-cellular biochemistry · 2026Review
- The Close Relationship between the Golgi Trafficking Machinery and Protein Glycosylation.Cells · 2020Review
- Maintaining order: COG complex controls Golgi trafficking, processing, and sorting.FEBS letters · 2019Review
- More than just sugars: Conserved oligomeric Golgi complex deficiency causes glycosylation-independent cellular defects.Traffic (Copenhagen, Denmark) · 2018Article
- COG Complex Complexities: Detailed Characterization of a Complete Set of HEK293T Cells Lacking Individual COG Subunits.Frontiers in cell and developmental biology · 2016Article
- Expression of functional Myc-tagged conserved oligomeric Golgi (COG) subcomplexes in mammalian cells.Methods in molecular biology (Clifton, N.J.) · 2015Article
- Target silencing of components of the conserved oligomeric Golgi complex impairs HIV-1 replication.Virus research · 2014Article
- Deficiency of the Cog8 subunit in normal and CDG-derived cells impairs the assembly of the COG and Golgi SNARE complexes.Traffic (Copenhagen, Denmark) · 2013Article
- Fluorescent microscopy as a tool to elucidate dysfunction and mislocalization of Golgi glycosyltransferases in COG complex depleted mammalian cells.Methods in molecular biology (Clifton, N.J.) · 2013Article
- Mislocalization of large ARF-GEFs as a potential mechanism for BFA resistance in COG-deficient cells.Experimental cell research · 2011Article
- Golgi glycosylation.Cold Spring Harbor perspectives in biology · 2011Review
- Cog2 null mutant CHO cells show defective sphingomyelin synthesis.The Journal of biological chemistry · 2010Article
- Defective GM3 synthesis in Cog2 null mutant CHO cells associates to mislocalization of lactosylceramide sialyltransferase in the Golgi complex.Neurochemical research · 2010Article
- Comparative analyses of the Conserved Oligomeric Golgi (COG) complex in vertebrates.BMC evolutionary biology · 2010Article
- Role of vesicle tethering factors in the ER-Golgi membrane traffic.FEBS letters · 2009Review
- Golgi function and dysfunction in the first COG4-deficient CDG type II patient.Human molecular genetics · 2009Article
- Structural basis for a human glycosylation disorder caused by mutation of the COG4 gene.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Direct interaction between the COG complex and the SM protein, Sly1, is required for Golgi SNARE pairing.The EMBO journal · 2009Article
- Role of the conserved oligomeric Golgi (COG) complex in protein glycosylation.Carbohydrate research · 2008Review
- Conserved oligomeric Golgi complex subunit 1 deficiency reveals a previously uncharacterized congenital disorder of glycosylation type II.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Two genetically distinct classes of low density lipoprotein (LDL) receptor-deficient Chinese hamster ovary cell mutants, ldlB and ldlC, exhibit nearly identical pleiotropic defects in multiple medial and trans Golgi-associated processes (Kingsley, D., K. F. Kozarsky, M. Segal, and M. Krieger. 1986. J. Cell Biol. 102:1576-1585). In these mutants, the synthesis of virtually all N- and O-linked glycoproteins and of the major lipid-linked oligosaccharides is abnormal. The abnormal glycosylation of LDL receptors in ldlB and ldlC cells results in their dramatically reduced stability and thus very low LDL receptor activity. We have cloned and sequenced a human cDNA (LDLC) which corrects the mutant phenotypes of ldlC, but not ldlB, cells. Unlike wild-type CHO or ldlB cells, ldlC cells had virtually no detectable endogenous LDLC mRNA, indicating that LDLC is likely to be the normal human homologue of the defective gene in ldlC cells. The predicted sequence of the human LDLC protein (ldlCp, approximately 83 kD) is not similar to that of any known proteins, and contains no major common structural motifs such as transmembrane domains or an ER translocation signal sequence. We have also determined the sequence of the Caenorhabditis elegans ldlCp by cDNA cloning and sequencing. Its similarity to that of human ldlCp suggests that ldlCp mediates a well-conserved cellular function. Immunofluorescence studies with anti-ldlCp antibodies in mammalian cells established that ldlCp is a peripheral Golgi protein whose association with the Golgi is brefeldin A sensitive. In ldlB cells, ldlCp was expressed at normal levels; however, it was not associated with the Golgi. Thus, a combination of somatic cell and molecular genetics has identified a previously unrecognized protein, ldlCp, which is required for multiple Golgi functions and whose peripheral association with the Golgi is both LDLB dependent and brefeldin A sensitive.
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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.