ArticleNature communications2019
GORAB scaffolds COPI at the trans-Golgi for efficient enzyme recycling and correct protein glycosylation.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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
31 citing papers in PubMed, 55 citations in OpenAlex.
- The Functions of RAB GTPases at the Golgi Complex.Sub-cellular biochemistry · 2026Review
- Siamese Twins: The Multimodular Mechanisms of Golgi Maturation and Glycan Synthesis Are Coupled at Their Core.Sub-cellular biochemistry · 2026Review
- Article
- SCYL1 deficiency in CALFAN syndrome is associated with ER stress and cell death.Disease models & mechanisms · 2025Article
- Review
- Targeting TGF-β signaling, oxidative stress, and cellular senescence rescues osteoporosis in gerodermia osteodysplastica.Aging cell · 2024Article
- Cant1 Affects Cartilage Proteoglycan Properties: Aggrecan and Decorin Characterization in a Mouse Model of Desbuquois Dysplasia Type 1.Biomolecules · 2024Article
- Review
- Rab6-mediated retrograde trafficking from the Golgi: the trouble with tubules.Small GTPases · 2023Review
- Vimentin intermediate filaments provide structural stability to the mammalian Golgi complex.Journal of cell science · 2023Article
- The factory, the antenna and the scaffold: the three-way interplay between the Golgi, cilium and extracellular matrix underlying tissue function.Biology open · 2023Review
- Overexpression of SCYL1 Is Associated with Progression of Breast Cancer.Current oncology (Toronto, Ont.) · 2022Article
- mTORC1 controls Golgi architecture and vesicle secretion by phosphorylation of SCYL1.Nature communications · 2022Article
- A glossary of plant cell structures: Current insights and future questions.The Plant cell · 2022Review
- Shared and specific functions of Arfs 1-5 at the Golgi revealed by systematic knockouts.The Journal of cell biology · 2022Article
- Supply chain logistics - the role of the Golgi complex in extracellular matrix production and maintenance.Journal of cell science · 2022Review
- Role of theFrontiers in cell and developmental biology · 2022Review
- COPB2 loss of function causes a coatopathy with osteoporosis and developmental delay.American journal of human genetics · 2021Article
- Golgi maturation-dependent glycoenzyme recycling controls glycosphingolipid biosynthesis and cell growth via GOLPH3.The EMBO journal · 2021Article
- The role of the Golgi apparatus in disease (Review).International journal of molecular medicine · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 7 institutions in 5 countries.
Funding
Abstract
COPI is a key mediator of protein trafficking within the secretory pathway. COPI is recruited to the membrane primarily through binding to Arf GTPases, upon which it undergoes assembly to form coated transport intermediates responsible for trafficking numerous proteins, including Golgi-resident enzymes. Here, we identify GORAB, the protein mutated in the skin and bone disorder gerodermia osteodysplastica, as a component of the COPI machinery. GORAB forms stable domains at the trans-Golgi that, via interactions with the COPI-binding protein Scyl1, promote COPI recruitment to these domains. Pathogenic GORAB mutations perturb Scyl1 binding or GORAB assembly into domains, indicating the importance of these interactions. Loss of GORAB causes impairment of COPI-mediated retrieval of trans-Golgi enzymes, resulting in a deficit in glycosylation of secretory cargo proteins. Our results therefore identify GORAB as a COPI scaffolding factor, and support the view that defective protein glycosylation is a major disease mechanism in gerodermia osteodysplastica.
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.