ArticleDevelopment (Cambridge, England)2016
Golgb1 regulates protein glycosylation and is crucial for mammalian palate development.
Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 63 citations in OpenAlex.
- GOLGB1 deficiency accelerates intervertebral disc degeneration by activating the MAPK pathway.Scientific reports · 2026Article
- Golgi Units as Modules in the Ribbon.Sub-cellular biochemistry · 2026Article
- Multiple golgins are required to support extracellular matrix secretion, modification, and assembly.The Journal of cell biology · 2025Article
- Prenatal growth patterns of the upper jaw complex with implications for laryngeal echolocation in bats.Journal of anatomy · 2025Article
- Dynamic movement of the Golgi unit and its glycosylation enzyme zones.Nature communications · 2024Article
- Deficiency ofInternational journal of molecular sciences · 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
- FGF9 Promotes Expression of HAS2 in Palatal Elevation via the Wnt/β-Catenin/TCF7L2 Pathway.Biomolecules · 2022Article
- The chromosome-scale genome of the raccoon dog: Insights into its evolutionary characteristics.iScience · 2022Article
- Pedigree-based study to identify GOLGB1 as a risk gene for bipolar disorder.Translational psychiatry · 2022Article
- Golgi Dysfunctions in Ciliopathies.Cells · 2022Review
- Revisiting the embryogenesis of lip and palate development.Oral diseases · 2022Review
- Orofacial Cleft and Mandibular Prognathism-Human Genetics and Animal Models.International journal of molecular sciences · 2022Review
- Novel investigations in retinoic-acid-induced cleft palate about the gut microbiome of pregnant mice.Frontiers in cellular and infection microbiology · 2022Article
- Golgin Subfamily A Member 5 Is Essential for Production of Extracellular Matrix Proteins during TGF-Stem cells international · 2022Article
- Methods of Palate Culture in Later Palatogenesis: Elevation, Horizontal Outgrowth, and Fusion.Methods in molecular biology (Clifton, N.J.) · 2022Article
- In-frame deletion of SPECC1L microtubule association domain results in gain-of-function phenotypes affecting embryonic tissue movement and fusion events.Human molecular genetics · 2021Article
- Getting Sugar Coating Right! The Role of the Golgi Trafficking Machinery in Glycosylation.Cells · 2021Review
- Giantin is required for intracellular N-terminal processing of type I procollagen.The Journal of cell biology · 2021Article
- Isolation and Time-Lapse Imaging of Primary Mouse Embryonic Palatal Mesenchyme Cells to Analyze Collective Movement Attributes.Journal of visualized experiments : JoVE · 2021Article
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
Cleft palate is a common major birth defect for which currently known causes account for less than 30% of pathology in humans. In this study, we carried out mutagenesis screening in mice to identify new regulators of palatogenesis. Through genetic linkage mapping and whole-exome sequencing, we identified a loss-of-function mutation in the Golgb1 gene that co-segregated with cleft palate in a new mutant mouse line. Golgb1 is a ubiquitously expressed large coiled-coil protein, also known as giantin, that is localized at the Golgi membrane. Using CRISPR/Cas9-mediated genome editing, we generated and analyzed developmental defects in mice carrying additional Golgb1 loss-of-function mutations, which supported a crucial requirement for Golgb1 in palate development. Through maxillary explant culture assays, we demonstrate that the Golgb1 mutant embryos have intrinsic defects in palatal shelf elevation. Just prior to the developmental stage of palatal shelf elevation in wild-type littermates, Golgb1 mutant embryos exhibit increased cell density, reduced hyaluronan accumulation and impaired protein glycosylation in the palatal mesenchyme. Together, these results demonstrate that, although it is a ubiquitously expressed Golgi-associated protein, Golgb1 has specific functions in protein glycosylation and tissue morphogenesis.
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.