ArticleJournal of neurochemistry2011
Knockout of G protein β5 impairs brain development and causes multiple neurologic abnormalities in mice.
Article in Journal of neurochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 58 citations in OpenAlex.
- Identification of Gβ5 Interactome Associated with Neuronal Development in Neuro-2a Cells through miniTurbo Proximity Labeling.ACS omega · 2026Article
- Mixed Segmental Uniparental Disomy of Chromosome 15q11-q1 Coexists with Homozygous Variant inGenes · 2025Article
- Gnb5 is a negative regulator of the BACE1-mediated Aβ generation and ameliorates cognitive deficits in a mouse model of Alzheimer's disease.PLoS biology · 2025Article
- Exploration of Epigenetic Mechanisms and Biomarkers Among Patients with Very-Late-Onset Schizophrenia-Like Psychosis.Neuropsychiatric disease and treatment · 2025Article
- Article
- The association of GNB5 with Alzheimer disease revealed by genomic analysis restricted to variants impacting gene function.American journal of human genetics · 2024Article
- Cell specific single viral vector CRISPR/Cas9 editing and genetically encoded tool delivery in the central and peripheral nervous systems.bioRxiv : the preprint server for biology · 2023Article
- Brain region-specific effects of nearly fixed sapiens-derived alleles.BMC genomic data · 2022Article
- Article
- Inhibition of G-protein signalling in cardiac dysfunction of intellectual developmental disorder with cardiac arrhythmia (IDDCA) syndrome.Journal of medical genetics · 2021Article
- Article
- Subtype-dependent regulation of Gβγ signalling.Cellular signalling · 2021Review
- Genetic characterization and long-term management of severely affected siblings with intellectual developmental disorder with cardiac arrhythmia syndrome.Molecular genetics and metabolism reports · 2020Article
- DNA methylation patterns of LINE-1 and Alu for pre-symptomatic dementia in type 2 diabetes.PloS one · 2020Article
- Severe Phenotype in a Patient With Homozygous 15q21.2 Microdeletion InvolvingFrontiers in genetics · 2020Article
- Review
- The expanding roles and mechanisms of G protein-mediated presynaptic inhibition.The Journal of biological chemistry · 2019Review
- GPCR regulation of secretion.Pharmacology & therapeutics · 2018Review
- Activation of β- and α2-adrenergic receptors stimulate tubulin polymerization and promote the association of Gβγ with microtubules in cultured NIH3T3 cells.Biochemical and biophysical research communications · 2018Article
- A High-Throughput Time-Resolved Fluorescence Energy Transfer Assay to Screen for Modulators of RGS7/Gβ5/R7BP Complex.Assay and drug development technologies · 2018Article
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 5 institutions in 1 country.
Funding
Abstract
Gβ5 is a divergent member of the signal-transducing G protein β subunit family encoded by GNB5 and expressed principally in brain and neuronal tissue. Among heterotrimeric Gβ isoforms, Gβ5 is unique in its ability to heterodimerize with members of the R7 subfamily of the regulator of G protein signaling proteins that contain G protein-γ like domains. Previous studies employing Gnb5 knockout (KO) mice have shown that Gβ5 is an essential stabilizer of such regulator of G protein signaling proteins and regulates the deactivation of retinal phototransduction and the proper functioning of retinal bipolar cells. However, little is known of the function of Gβ5 in the brain outside the visual system. We show here that mice lacking Gβ5 have a markedly abnormal neurologic phenotype that includes impaired development, tiptoe-walking, motor learning and coordination deficiencies, and hyperactivity. We further show that Gβ5-deficient mice have abnormalities of neuronal development in cerebellum and hippocampus. We find that the expression of both mRNA and protein from multiple neuronal genes is dysregulated in Gnb5 KO mice. Taken together with previous observations from Gnb5 KO mice, our findings suggest a model in which Gβ5 regulates dendritic arborization and/or synapse formation during development, in part by effects on gene expression.
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.