ArticleMolecular biology reports2024
Expression analysis of type I ARF small GTPases ARF1-3 during mouse brain development.
Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- ARF1-Related Diseases in China: The Initial Study of Phenotype and Molecular Profile.Journal of cellular and molecular medicine · 2025Article
- Distribution analysis of RAB11A and RAB11B, small GTP-binding proteins, in mice.Molecular biology reports · 2025Article
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
backgroundARF (ADP-ribosylation factor) GTPases are major regulators of intracellular trafficking, and classified into 3 groups (Type I - III), among which the type I group members, ARF1 and 3, are responsible genes for neurodevelopmental disorders.
methodsIn this study, we analysed the expression of Type I ARFs ARF1-3 during mouse brain development using biochemical and morphological methods.
resultsWestern blotting analyses revealed that ARF1-3 are weakly expressed in the mouse brain at embryonic day 13 and gradually increase until postnatal day 30. ARF1-3 appear to be abundantly expressed in various telencephalon regions. Biochemical fractionation studies detected ARF1-3 in the synaptosome fraction of cortical neurons containing both pre- and post-synapses, however ARF1-3 were not observed in post-synaptic compartments. In immunohistochemical analyses, ARF1-3 appeared to be distributed in the cytoplasm and dendrites of cortical and hippocampal neurons as well as in the cerebellar molecular layer including dendrites of Purkinje cells and granule cell axons. Immunofluorescence in primary cultured hippocampal neurons revealed that ARF1-3 are diffusely distributed in the cytoplasm and dendrites with partial colocalization with a pre-synaptic marker, synaptophysin.
conclusionsOverall, our results support the notion that ARF1-3 could participate in vesicle trafficking both in the dendritic shaft (excluding spines) and axon terminals (pre-synaptic compartments).
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