ArticleMolecular biology of the cell1997
Sec31 encodes an essential component of the COPII coat required for transport vesicle budding from the endoplasmic reticulum.
Article in Molecular biology of the cell, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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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.
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Who cites it
69 citing papers in PubMed, 146 citations in OpenAlex.
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- Less is better: various means to reduce protein load in the endoplasmic reticulum.The FEBS journal · 2025Review
- Characterization and functional analysis ofmBio · 2024Article
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- COPII cage assembly factor Sec13 integrates information flow regulating endomembrane function in response to human variation.Scientific reports · 2024Article
- The ER-Golgi transport of influenza virus through NS1-Sec13 association during virus replication.Microbiology spectrum · 2024Article
- Cargo selection in endoplasmic reticulum-to-Golgi transport and relevant diseases.The Journal of clinical investigation · 2023Review
- The alternative splicing landscape of a coral reef fish during a marine heatwave.Ecology and evolution · 2022Article
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- Regulation of glial size by eicosapentaenoic acid through a novel Golgi apparatus mechanism.PLoS biology · 2020Article
- Consequences of mutations in the genes of the ER export machinery COPII in vertebrates.Cell stress & chaperones · 2020Review
- Export Control: Post-transcriptional Regulation of the COPII Trafficking Pathway.Frontiers in cell and developmental biology · 2020Review
- Twenty-five years after coat protein complex II.Molecular biology of the cell · 2020Article
- Roles of Membrane and Vesicular Traffic in Regulation of the Hippo Pathway.Frontiers in cell and developmental biology · 2019Review
- Visualizing Mutation-Specific Differences in the Trafficking-Deficient Phenotype of Kv11.1 Proteins Linked to Long QT Syndrome Type 2.Frontiers in physiology · 2018Article
- TFG facilitates outer coat disassembly on COPII transport carriers to promote tethering and fusion with ER-Golgi intermediate compartments.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Secretory COPII Protein SEC31B Is Required for Pollen Wall Development.Plant physiology · 2016Article
9 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The COPII vesicle coat protein promotes the formation of endoplasmic reticulum- (ER) derived transport vesicles that carry secretory proteins to the Golgi complex in Saccharomyces cerevisiae. This coat protein consists of Sar1p, the Sec23p protein complex containing Sec23p and Sec24p, and the Sec13p protein complex containing Sec13p and a novel 150-kDa protein, p150. Here, we report the cloning and characterization of the p150 gene. p150 is encoded by an essential gene. Depletion of this protein in vivo blocks the exit of secretory proteins from the ER and causes an elaboration of ER membranes, indicating that p150 is encoded by a SEC gene. Additionally, overproduction of the p150 gene product compromises the growth of two ER to Golgi sec mutants: sec16-2 and sec23-1. p150 is encoded by SEC31, a gene isolated in a genetic screen for mutations that accumulate unprocessed forms of the secretory protein alpha-factor. The sec31-1 mutation was mapped by gap repair, and sequence analysis revealed an alanine to valine change at position 1239, near the carboxyl terminus. Sec31p is a phosphoprotein and treatment of the Sec31p-containing fraction with alkaline phosphatase results in a 50-75% inhibition of transport vesicle formation activity in an ER membrane budding assay.
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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.