ArticleExperimental cell research2011
Mislocalization of large ARF-GEFs as a potential mechanism for BFA resistance in COG-deficient cells.
Article in Experimental cell research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- COG Complex in Golgi Trafficking and Glycosylation.Sub-cellular biochemistry · 2026Review
- Golgi inCOGnito: From vesicle tethering to human disease.Biochimica et biophysica acta. General subjects · 2020Review
- A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes.Diabetes · 2020Article
- TRAPPC13 modulates autophagy and the response to Golgi stress.Journal of cell science · 2017Article
- Rewiring of cellular membrane homeostasis by picornaviruses.Journal of virology · 2014Review
- Further characterization of ATP6V0A2-related autosomal recessive cutis laxa.Human genetics · 2012Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Defects in subunits of the conserved oligomeric Golgi (COG) complex represent a growing subset of congenital disorders of glycosylation (CDGs). In addition to altered protein glycosylation and vesicular trafficking, Cog-deficient patient fibroblasts exhibit a striking delay in the Golgi-disrupting effects of brefeldin A (BFA). Despite the diagnostic value of this BFA resistance, the molecular basis of this response is not known. To investigate potential mechanisms of resistance, we analyzed the localization of the large ARF-GEF, GBF1, in several Cog-deficient cell lines. Our results revealed mislocalization of GBF1 to non-Golgi compartments, in particular the ERGIC, within these cells. Biochemical analysis of GBF1 in control and BFA-treated fibroblasts demonstrated that the steady-state level and membrane recruitment is not substantially affected by COG deficiency, supporting a role for the COG complex in the localization but not membrane association of GBF1. We also showed that pretreatment of fibroblasts with bafilomycin resulted in a GBF1-independent BFA resistance that appears additive with the resistance associated with COG deficiency. These data provide new insight into the mechanism of BFA resistance in Cog-deficient cells by suggesting a role for impaired ARF-GEF localization.
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