ArticleTraffic (Copenhagen, Denmark)2006
Sec16 defines endoplasmic reticulum exit sites and is required for secretory cargo export in mammalian cells.
Article in Traffic (Copenhagen, Denmark), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers.
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.
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Who cites it
131 citing papers in PubMed, 239 citations in OpenAlex.
- Inhibition of TFG function causes hereditary axon degeneration by impairing endoplasmic reticulum structure.Proceedings of the National Academy of Sciences of the United States of America · 2013Trial
- The Golgi vesicle tether p115 can bind directly to the ER exit site organiser Sec16A.Journal of cell science · 2026Article
- Physiological implications of phase separation in vesicle organization and trafficking.BMC biology · 2026Review
- Construction of pathogenic Sec16a mutation mouse model using CRISPR/Cas9.Animal models and experimental medicine · 2026Article
- Models of Intracellular Transport: Contradictions and Current Understanding.Sub-cellular biochemistry · 2026Review
- Dynamic O-GlcNAcylation of Sec23-interacting protein regulates COPII function.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
- Tissue-specific SEC31A alternative splicing is regulated by RBM47 and controls lipid transport.RNA (New York, N.Y.) · 2025Article
- Genomics reveals eleven obesity endotypes with distinct biological and phenotypic signatures.medRxiv : the preprint server for health sciences · 2025Article
- Article
- Cell-intrinsic insulin signaling defects in human iPS cell-derived hepatocytes in type 2 diabetes.The Journal of clinical investigation · 2025Article
- Plant-specific tail-anchored coiled-coil protein MAG3 stabilizes Golgi-associated ERESs to facilitate protein exit from the ER.Communications biology · 2025Article
- Less is better: various means to reduce protein load in the endoplasmic reticulum.The FEBS journal · 2025Review
- Sec23IP recruits VPS13B/COH1 to ER exit site-Golgi interface for tubular ERGIC formation.The Journal of cell biology · 2024Article
- TDP43 aggregation at ER-exit sites impairs ER-to-Golgi transport.Nature communications · 2024Article
- Small GTPase ActIvitY ANalyzing (SAIYAN) system: A method to detect GTPase activation in living cells.The Journal of cell biology · 2024Article
- De novo lipid synthesis and polarized prenylation drive cell invasion through basement membrane.The Journal of cell biology · 2024Article
- TFG regulates inner COPII coat recruitment to facilitate anterograde secretory protein transport.Molecular biology of the cell · 2024Article
- The Golgi Apparatus: A Key Player in Innate Immunity.International journal of molecular sciences · 2024Review
- HTRA1-driven detachment of type I collagen from endoplasmic reticulum contributes to myocardial fibrosis in dilated cardiomyopathy.Journal of translational medicine · 2024Article
71 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
5 authors at 1 institution in 1 country.
Funding
Abstract
The selective export of proteins and lipids from the endoplasmic reticulum (ER) is mediated by the coat protein complex II (COPII) that assembles onto the ER membrane. In higher eukaryotes, COPII proteins assemble at discrete sites on the membrane known as ER exit sites (ERES). Here, we identify Sec16 as the protein that defines ERES in mammalian cells. Sec16 localizes to ERES independent of Sec23/24 and Sec13/31. Overexpression, and to a lesser extent, small interfering RNA depletion of Sec16, both inhibit ER-to-Golgi transport suggesting that Sec16 is required in stoichiometric amounts. Sar1 activity is required to maintain the localization of Sec16 at discrete locations on the ER membrane, probably through preventing its dissociation. Our data suggest that Sar1-GTP-dependent assembly of Sec16 on the ER membrane forms an organized scaffold defining an ERES.
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What OpenQuestion holds
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.