ArticleJournal of cell science2009
Organisation of human ER-exit sites: requirements for the localisation of Sec16 to transitional ER.
Article in Journal of cell science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
105 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Stay in touch with the endoplasmic reticulum.Science China. Life sciences · 2024Pooled it
- EMT activates ER-to-Golgi trafficking through upregulation of REEP2 to promote lung cancer progression.Research square · 2026Article
- Hepatic SEC16B regulates lipid homeostasis by coordinating VLDL secretion and lipid droplet expansion.The Journal of clinical investigation · 2026Article
- The Golgi vesicle tether p115 can bind directly to the ER exit site organiser Sec16A.Journal of cell science · 2026Article
- Tissue-selective COPII modulator SEC16B aggravates cardiovascular disease by promoting lipid export.The EMBO journal · 2026Article
- Physiological implications of phase separation in vesicle organization and trafficking.BMC biology · 2026Review
- Beyond Vesicular Traffic: The ERES as the Gateway for Biosynthetic Secretion.Sub-cellular biochemistry · 2026Review
- Plant Golgi and GECCO: The Universality of ER-Golgi Interface.Sub-cellular biochemistry · 2026Review
- EMT activates ER-to-Golgi trafficking through upregulation of REEP2 to promote lung cancer progression.bioRxiv : the preprint server for biology · 2025Article
- Towards a unified framework for the function of endoplasmic reticulum exit sites.Nature reviews. Molecular cell biology · 2025Review
- The short isoform of Tango1 is dispensable for zebrafish survival but is required for skeletal patterning and integrity.Biology open · 2025Article
- Tissue-specific SEC31A alternative splicing is regulated by RBM47 and controls lipid transport.RNA (New York, N.Y.) · 2025Article
- Article
- Plant-specific tail-anchored coiled-coil protein MAG3 stabilizes Golgi-associated ERESs to facilitate protein exit from the ER.Communications biology · 2025Article
- Potential ER tubular lumen sensing by intrinsically disordered regions.Journal of cell science · 2025Article
- Remodeling of the secretory pathway is coordinated withiScience · 2024Article
- SEC16A Variants Predispose to Chronic Pancreatitis by Impairing ER-to-Golgi Transport and Inducing ER Stress.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Protein condensates in the the secretory pathway: Unraveling biophysical interactions and function.Biophysical journal · 2024Review
- HTRA1-driven detachment of type I collagen from endoplasmic reticulum contributes to myocardial fibrosis in dilated cardiomyopathy.Journal of translational medicine · 2024Article
- ER exit in physiology and disease.Frontiers in molecular biosciences · 2024Review
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
The COPII complex mediates the selective incorporation of secretory cargo and relevant machinery into budding vesicles at specialised sites on the endoplasmic reticulum membrane called transitional ER (tER). Here, we show using confocal microscopy, immunogold labelling of ultrathin cryosections and electron tomography that in human cells at steady state, Sec16 localises to cup-like structures of tER that are spatially distinct from the localisation of other COPII coat components. We show that Sec16 defines the tER, whereas Sec23-Sec24 and Sec13-Sec31 define later structures that precede but are distinct from the intermediate compartment. Steady-state localisation of Sec16 is independent of the localisation of downstream COPII components Sec23-Sec24 and Sec13-Sec31. Sec16 cycles on and off the membrane at a slower rate than other COPII components with a greater immobile fraction. We define the region of Sec16A that dictates its robust localisation of tER membranes and find that this requires both a highly charged region as well as a central domain that shows high sequence identity between species. The central conserved domain of Sec16 binds to Sec13 linking tER membrane localisation with COPII vesicle formation. These data are consistent with a model where Sec16 acts as a platform for COPII assembly at ERES.
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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.