ArticleThe Journal of cell biology1999
ER/Golgi intermediates acquire Golgi enzymes by brefeldin A-sensitive retrograde transport in vitro.
Article in The Journal of cell biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 38 citations in OpenAlex.
- Syntaxin-5's flexibility in SNARE pairing supports Golgi functions.Traffic (Copenhagen, Denmark) · 2023Article
- CHIP/STUB1 Ubiquitin Ligase Functions as a Negative Regulator of ErbB2 by Promoting Its Early Post-Biosynthesis Degradation.Cancers · 2021Article
- Genome-Wide Analysis of Multidrug and Toxic Compound Extrusion (G3 (Bethesda, Md.) · 2018Article
- Irradiation-induced protein inactivation reveals Golgi enzyme cycling to cell periphery.Journal of cell science · 2012Article
- Golgi and related vesicle proteomics: simplify to identify.Cold Spring Harbor perspectives in biology · 2011Review
- Meningococcal porin PorB prevents cellular apoptosis in a toll-like receptor 2- and NF-kappaB-independent manner.Infection and immunity · 2010Article
- Regulation of microtubule-dependent recycling at the trans-Golgi network by Rab6A and Rab6A'.Molecular biology of the cell · 2005Article
- Nck-dependent activation of extracellular signal-regulated kinase-1 and regulation of cell survival during endoplasmic reticulum stress.Molecular biology of the cell · 2004Article
- Localization of p24 putative cargo receptors in the early secretory pathway depends on the biosynthetic activity of the cell.The Biochemical journal · 2001Article
- Stoichiometry and kinetics of transport vesicle fusion with Golgi membranes.EMBO reports · 2001Article
- Asymmetric requirements for a Rab GTPase and SNARE proteins in fusion of COPII vesicles with acceptor membranes.The Journal of cell biology · 2000Article
- Role of tetanus neurotoxin insensitive vesicle-associated membrane protein in membrane domains transport and homeostasis.Cellular logisticsArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secretory proteins exit the ER in transport vesicles that fuse to form vesicular tubular clusters (VTCs) which move along microtubule tracks to the Golgi apparatus. Using the well-characterized in vitro approach to study the properties of Golgi membranes, we determined whether the Golgi enzyme NAGT I is transported to ER/Golgi intermediates. Secretory cargo was arrested at distinct steps of the secretory pathway of a glycosylation mutant cell line, and in vitro complementation of the glycosylation defect was determined. Complementation yield increased after ER exit of secretory cargo and was optimal when transport was blocked at an ER/Golgi intermediate step. The rapid drop of the complementation yield as secretory cargo progresses into the stack suggests that Golgi enzymes are preferentially targeted to ER/Golgi intermediates and not to membranes of the Golgi stack. Two mechanisms for in vitro complementation could be distinguished due to their different sensitivities to brefeldin A (BFA). Transport occurred either by direct fusion of preexisting transport intermediates with ER/Golgi intermediates, or it occurred as a BFA-sensitive and most likely COP I-mediated step. Direct fusion of ER/Golgi intermediates with cisternal membranes of the Golgi stack was not observed under these conditions.
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Registered trials
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.