ArticlePloS one2016
C3G/Rapgef1 Is Required in Multipolar Neurons for the Transition to a Bipolar Morphology during Cortical Development.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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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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.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Rapgef1 paralog-mediated regulation of Wnt/β-catenin signaling orchestrates early embryo tissue patterning and morphogenesis.Cell communication and signaling : CCS · 2026Article
- Deletion of C3G in hepatocytes impairs full liver maturation and alters glucose homeostasis.Cell death & disease · 2025Article
- Cadherin-6 controls neuronal migration during mouse neocortical development via an integrin-mediated pathway.The FEBS journal · 2025Article
- A novel long non-coding RNA, PICSAR, promotes thyroid cancer progression through the hsa-miR-320A/hsa-miR-485/RAPGEFL1 axis.Medical oncology (Northwood, London, England) · 2025Article
- Review
- Extracellular vesicle signatures from eye lavage as novel non-invasive biomarkers for hypoxic ischaemic insult-findings from a neonatal mouse model.Frontiers in medical technology · 2025Article
- Pip5k1γ regulates axon formation by limiting Rap1 activity.Life science alliance · 2024Article
- Review
- Delayed cortical development in mice with a neural specific deletion of β1 integrin.Frontiers in neuroscience · 2023Article
- C3G Protein, a New Player in Glioblastoma.International journal of molecular sciences · 2021Review
- C3G downregulation induces the acquisition of a mesenchymal phenotype that enhances aggressiveness of glioblastoma cells.Cell death & disease · 2021Article
- Expression of a novel brain specific isoform of C3G is regulated during development.Scientific reports · 2020Article
- C3G contributes to platelet activation and aggregation by regulating major signaling pathways.Signal transduction and targeted therapy · 2020Article
- Vitronectin is Involved in the Morphological Transition of Neurites in Retinoic Acid-Induced Neurogenesis of Neuroblastoma Cell Line Neuro2a.Neurochemical research · 2019Article
- Article
- C3G, through its GEF activity, induces megakaryocytic differentiation and proplatelet formation.Cell communication and signaling : CCS · 2018Article
- Development and characterization of a novel monoclonal antibody that recognizes an epitope in the central protein interaction domain of RapGEF1 (C3G).Molecular biology reports · 2018Article
- Rap1 GTPase promotes coordinated collective cell migration in vivo.Molecular biology of the cell · 2018Article
- Mutations in Vps15 perturb neuronal migration in mice and are associated with neurodevelopmental disease in humans.Nature neuroscience · 2018Article
- Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The establishment of a polarized morphology is essential for the development and function of neurons. During the development of the mammalian neocortex, neurons arise in the ventricular zone (VZ) from radial glia cells (RGCs) and leave the VZ to generate the cortical plate (CP). During their migration, newborn neurons first assume a multipolar morphology in the subventricular zone (SVZ) and lower intermediate zone (IZ). Subsequently, they undergo a multi-to-bipolar (MTB) transition to become bipolar in the upper IZ by developing a leading process and a trailing axon. The small GTPases Rap1A and Rap1B act as master regulators of neural cell polarity in the developing mouse neocortex. They are required for maintaining the polarity of RGCs and directing the MTB transition of multipolar neurons. Here we show that the Rap1 guanine nucleotide exchange factor (GEF) C3G (encoded by the Rapgef1 gene) is a crucial regulator of the MTB transition in vivo by conditionally inactivating the Rapgef1 gene in the developing mouse cortex at different time points during neuronal development. Inactivation of C3G results in defects in neuronal migration, axon formation and cortical lamination. Live cell imaging shows that C3G is required in cortical neurons for both the specification of an axon and the initiation of radial migration by forming a leading process.
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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.