ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
RIM3γ and RIM4γ are key regulators of neuronal arborization.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 22 citations in OpenAlex.
- Dissecting the propensity of RIM1 subdomains to form phase condensates.Scientific reports · 2026Article
- Antisense oligonucleotides to KIF1A polymorphisms expand targets and rescue patient-derived neurons in vitro.Nature communications · 2026Article
- Abnormal α-synuclein binds to synaptotagmin 13, impairing extracellular vesicle release in synucleinopathies.Translational neurodegeneration · 2025Article
- Ste20-like Kinase Is Critical for Inhibitory Synapse Maintenance and Its Deficiency Confers a Developmental Dendritopathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Synaptic ribbons foster active zone stability and illumination-dependent active zone enrichment of RIM2 and Cav1.4 in photoreceptor synapses.Scientific reports · 2020Article
- Genetic and Epigenetic Etiology Underlying Autism Spectrum Disorder.Journal of clinical medicine · 2020Review
- RIM is essential for stimulated but not spontaneous somatodendritic dopamine release in the midbrain.eLife · 2019Article
- Both rare and common genetic variants contribute to autism in the Faroe Islands.NPJ genomic medicine · 2019Article
- Coupling the Structural and Functional Assembly of Synaptic Release Sites.Frontiers in neuroanatomy · 2018Review
- Analysis of RIM Expression and Function at Mouse Photoreceptor Ribbon Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Rab Interacting Molecules 2 and 3 Directly Interact with the Pore-Forming CaFrontiers in cellular neuroscience · 2017Article
- Emerging Synaptic Molecules as Candidates in the Etiology of Neurological Disorders.Neural plasticity · 2017Review
- Severely impaired hippocampal neurogenesis associates with an early serotonergic deficit in a BAC α-synuclein transgenic rat model of Parkinson's disease.Neurobiology of disease · 2016Article
- Rab3-interacting molecules 2α and 2β promote the abundance of voltage-gated CaV1.3 Ca2+ channels at hair cell active zones.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The large isoforms of the Rab3 interacting molecule (RIM) family, RIM1α/β and RIM2α/β, have been shown to be centrally involved in mediating presynaptic active zone function. The RIM protein family contains two additional small isoforms, RIM3γ and RIM4γ, which are composed only of the RIM-specific C-terminal C2B domain and varying N-terminal sequences and whose function remains to be elucidated. Here, we report that both, RIM3γ and RIM4γ, play an essential role for the development of neuronal arborization and of dendritic spines independent of synaptic function. γ-RIM knock-down in rat primary neuronal cultures and in vivo resulted in a drastic reduction in the complexity of neuronal arborization, affecting both axonal and dendritic outgrowth, independent of the time point of γ-RIM downregulation during dendrite development. Rescue experiments revealed that the phenotype is caused by a function common to both γ-RIMs. These findings indicate that γ-RIMs are involved in cell biological functions distinct from the regulation of synaptic vesicle exocytosis and play a role in the molecular mechanisms controlling the establishment of dendritic complexity and axonal outgrowth.
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.