ReviewInternational journal of molecular sciences2018
Rho GTPases in Intellectual Disability: From Genetics to Therapeutic Opportunities.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed.
- Functional Mapping of Neurodevelopmental Disease Pathways to Key Neurodevelopmental Processes Represented in the Developmental Neurotoxicity In Vitro Testing Battery.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- DNA methylation signatures associated with early-onset schizophrenia in Chinese patients.Translational psychiatry · 2026Article
- Systems-level analysis uncovers eight hub genes and a resveratrol-based therapeutic strategy for ischemic stroke.Frontiers in pharmacology · 2026Article
- RhoA/ROCK2 signaling pathway regulates Mn-induced alterations in tight junction proteins leading to cognitive dysfunction in mice.Current research in toxicology · 2025Article
- Ras, RhoA, and vascular pharmacology in neurodevelopment and aging.Neurochemistry international · 2024Review
- Article
- Presenilin2 D439A Mutation Induces Dysfunction of Mitochondrial Fusion/Fission Dynamics and Abnormal Regulation of GTPase Activity.Molecular neurobiology · 2024Article
- Burden of Rare Copy Number Variants in Microcephaly: A Brazilian Cohort of 185 Microcephalic Patients and Review of the Literature.Journal of autism and developmental disorders · 2024Review
- PPP1R14B as a potential biomarker for the identification of diagnosis and prognosis affecting tumor immunity, proliferation and migration in prostate cancer.Journal of Cancer · 2024Article
- Investigating recovery after a spontaneous intracerebral haemorrhage in zebrafish larvae.Brain communications · 2024Article
- Recombinant Slit2 suppresses neuroinflammation and Cdc42-mediated brain infiltration of peripheral immune cells via Robo1-srGAP1 pathway in a rat model of germinal matrix hemorrhage.Journal of neuroinflammation · 2023Article
- A Systematic Compilation of Human SH3 Domains: A Versatile Superfamily in Cellular Signaling.Cells · 2023Review
- Impact of IDH Mutations, the 1p/19q Co-Deletion and the G-CIMP Status on Alternative Splicing in Diffuse Gliomas.International journal of molecular sciences · 2023Article
- A Structural Network Analysis of Neuronal ArhGAP21/23 Interactors by Computational Modeling.ACS omega · 2023Article
- Differentiation of neurosphere after transplantation into the damaged spinal cord.Journal of medicine and life · 2023Article
- Network pharmacology reveals that Berberine may function against Alzheimer's disease via the AKT signaling pathway.Frontiers in neuroscience · 2023Article
- Presynaptic Rac1 controls synaptic strength through the regulation of synaptic vesicle priming.eLife · 2022Article
- Variant-specific changes in RAC3 function disrupt corticogenesis in neurodevelopmental phenotypes.Brain : a journal of neurology · 2022Article
- Review
- RhoA Signaling in Neurodegenerative Diseases.Cells · 2022Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rho-class small GTPases are implicated in basic cellular processes at nearly all brain developmental steps, from neurogenesis and migration to axon guidance and synaptic plasticity. GTPases are key signal transducing enzymes that link extracellular cues to the neuronal responses required for the construction of neuronal networks, as well as for synaptic function and plasticity. Rho GTPases are highly regulated by a complex set of activating (GEFs) and inactivating (GAPs) partners, via protein:protein interactions (PPI). Misregulated RhoA, Rac1/Rac3 and cdc42 activity has been linked with intellectual disability (ID) and other neurodevelopmental conditions that comprise ID. All genetic evidences indicate that in these disorders the RhoA pathway is hyperactive while the Rac1 and cdc42 pathways are consistently hypoactive. Adopting cultured neurons for in vitro testing and specific animal models of ID for in vivo examination, the endophenotypes associated with these conditions are emerging and include altered neuronal networking, unbalanced excitation/inhibition and altered synaptic activity and plasticity. As we approach a clearer definition of these phenotype(s) and the role of hyper- and hypo-active GTPases in the construction of neuronal networks, there is an increasing possibility that selective inhibitors and activators might be designed via PPI, or identified by screening, that counteract the misregulation of small GTPases and result in alleviation of the cognitive condition. Here we review all knowledge in support of this possibility.
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