ArticleMolecular biology of the cell2007
Two mammalian Sec16 homologues have nonredundant functions in endoplasmic reticulum (ER) export and transitional ER organization.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
96 citing papers in PubMed, 1 synthesis or guideline pooled it, 154 citations in OpenAlex.
- A meta-analysis and polygenic score study identifies novel genetic markers for waist-hip ratio in African populations.Obesity (Silver Spring, Md.) · 2024Pooled it
- SEC16B identified as a regulator of VLDL secretion and lipid accumulation in the liver.The Journal of clinical investigation · 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
- Construction of pathogenic Sec16a mutation mouse model using CRISPR/Cas9.Animal models and experimental medicine · 2026Article
- Phosphorylation-coupled autoregulation of TANGO1 and Sec16A maintains functional ER exit sites.Nature communications · 2025Article
- Identification of SEC16B as a novel regulator of glucose homeostasis.Diabetologia · 2025Article
- Potential ER tubular lumen sensing by intrinsically disordered regions.Journal of cell science · 2025Article
- Endoplasmic reticulum exit sites are segregated for secretion based on cargo size.Developmental cell · 2024Article
- SEC16A Variants Predispose to Chronic Pancreatitis by Impairing ER-to-Golgi Transport and Inducing ER Stress.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The Golgi Apparatus: A Key Player in Innate Immunity.International journal of molecular sciences · 2024Review
- Nutrient deprivation alters the rate of COPII subunit recruitment at ER subdomains to tune secretory protein transport.Nature communications · 2023Article
- Endoplasmic reticulum network heterogeneity guides diffusive transport and kinetics.Biophysical journal · 2023Article
- The Sar1 GTPase is dispensable for COPII-dependent cargo export from the ER.Cell reports · 2023Article
- Bi-allelic mutation in SEC16B alters collagen trafficking and increases ER stress.EMBO molecular medicine · 2023Article
- Article
- Stress-induced phase separation of ERES components into Sec bodies precedes ER exit inhibition in mammalian cells.Journal of cell science · 2022Article
- Pathogenic variants of sphingomyelin synthase SMS2 disrupt lipid landscapes in the secretory pathway.eLife · 2022Article
- QTL-mapping in the obese Berlin Fat Mouse identifies additional candidate genes for obesity and fatty liver disease.Scientific reports · 2022Article
36 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Budding yeast Sec16 is a large peripheral endoplasmic reticulum (ER) membrane protein that functions in generating COPII transport vesicles and in clustering COPII components at transitional ER (tER) sites. Sec16 interacts with multiple COPII components. Although the COPII assembly pathway is evolutionarily conserved, Sec16 homologues have not been described in higher eukaryotes. Here, we show that mammalian cells contain two distinct Sec16 homologues: a large protein that we term Sec16L and a smaller protein that we term Sec16S. These proteins localize to tER sites, and an N-terminal region of each protein is necessary and sufficient for tER localization. The Sec16L and Sec16S genes are both expressed in every tissue examined, and both proteins are required in HeLa cells for ER export and for normal tER organization. Sec16L resembles yeast Sec16 in having a C-terminal conserved domain that interacts with the COPII coat protein Sec23, but Sec16S lacks such a C-terminal conserved domain. Immunoprecipitation data indicate that Sec16L and Sec16S are each present at multiple copies in a heteromeric complex. We infer that mammalian cells have preserved and extended the function of Sec16.
Indexed as
Identifiers
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.