ArticlePloS one2012
Golgi disruption and early embryonic lethality in mice lacking USO1.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- The Golgi vesicle tether p115 can bind directly to the ER exit site organiser Sec16A.Journal of cell science · 2026Article
- Conditional knockout mouse model demonstrates that Copa expression is required for viability in development and adulthood.Biochemical and biophysical research communications · 2025Article
- Characterization and functional analysis ofmBio · 2024Article
- Cysteinyl-specialized proresolving mediators link resolution of infectious inflammation and tissue regeneration via TRAF3 activation.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Golgi Apparatus May Be a Potential Therapeutic Target for Apoptosis-Related Neurological Diseases.Frontiers in cell and developmental biology · 2020Review
- Golgb1 regulates protein glycosylation and is crucial for mammalian palate development.Development (Cambridge, England) · 2016Article
- Intracellular Golgi Complex organization reveals tissue specific polarity during zebrafish embryogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2016Article
- GOLGA2, encoding a master regulator of golgi apparatus, is mutated in a patient with a neuromuscular disorder.Human genetics · 2016Article
- Emerging Insights into the Roles of Membrane Tethers from Analysis of Whole Organisms: The Tip of an Iceberg?Frontiers in cell and developmental biology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Golgins are a family of long rod-like proteins characterized by the presence of central coiled-coil domains. Members of the golgin family have important roles in membrane trafficking, where they function as tethering factors that capture transport vesicles and facilitate membrane fusion. Golgin family members also have essential roles in maintaining the organization of the Golgi apparatus. Knockdown of individual golgins in cultured cells resulted in the disruption of the Golgi structure and the dispersal of Golgi marker proteins throughout the cytoplasm. However, these cellular phenotypes have not always been recapitulated in vivo. For example, embryonic development proceeds much further than expected and Golgi disruption was observed in only a subset of cell types in mice lacking the ubiquitously expressed golgin GMAP-210. Cell-type specific functional compensation among golgins may explain the absence of global cell lethality when a ubiquitously expressed golgin is missing. In this study we show that functional compensation does not occur for the golgin USO1. Mice lacking this ubiquitously expressed protein exhibit disruption of Golgi structure and early embryonic lethality, indicating that USO1 is indispensable for early embryonic development.
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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.