Ask about this productRelated genes to: GABRG3 Blocking Peptide
- Gene:
- GABRG3 NIH gene
- Name:
- gamma-aminobutyric acid type A receptor gamma3 subunit
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 15q12
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-15
- Date modifiied:
- 2016-02-04
Related products to: GABRG3 Blocking Peptide
Related articles to: GABRG3 Blocking Peptide
- Brain-derived neurotrophic factor (BDNF) is a master regulator of neuronal differentiation and inhibitory circuit maturation in the mammalian brain. Yet, its downstream mediators in distinct neuronal populations remain incompletely defined. Here, we identify mitogen- and stress-activated kinase 1 (MSK1) as a critical mediator of BDNF signalling during postnatal striatal development. MSK1 expression predominates in GABAergic neurons across the cortex and striatum, with region-specific dynamics: MSK1 expression in cortical GABAergic interneurons declines from postnatal day 5 (P5) to day 30 (P30), while expression in striatal GABAergic medium spiny neurons (MSNs) persists into adulthood. Using a novel Msk1 KO mouse model, generated by deleting exon IV of Msk1, we find that striatal volume and MSN dendritic complexity decrease by P60, without cortical neuron alterations, underscoring MSK1´s striatal-specific role. Mechanistically, MSK1 drives BDNF-induced MeCP2 phosphorylation at serine 421 in MSNs via MAPK/ERK, independently of CaMKII, forming a nuclear complex with MeCP2, thus amplifying MSK1´s role in transcriptional regulation. This MSK1-MeCP2 signalling is also involved in BDNF-dependent and independent morphological developmental processes of cultured striatal neurons. Accordingly, Msk1 KO striatum shows dysregulated GABAergic (Gad1, Gabrg3) and dopaminergic (Drd1, Drd2, Drd3) gene expression, mirroring profiles in MeCP2 deficient models. Behaviourally, Msk1 KO mice display hypersociability, impaired nest-building, and increased depressive-like behaviour in the forced swimming test, contributing to striatal circuit dysfunction. These findings link MSK1-mediated molecular disruptions to inhibitory circuit imbalances and behaviours reminiscent of psychiatric disorders, positioning MSK1 as a potential therapeutic target for neurodevelopmental and psychiatric disorders, including those associated with MeCP2 dysfunction. - Source: PubMed
Publication date: 2026/05/18
Varela-Andrés NataliaHernández-Del Caño CarlosCebrián-León AlejandroBlanco AdriánLos Arcos-López de Pariza IzaskunFernández Del Campo Inés SGarcía-Losada SandraArévalo Juan CarlosSánchez-Martín ManuelBajo-Grañeras RaquelMartín RicardoSánchez-Aguilera AlbertoMerchán Miguel ADeogracias Rubén - has traditionally been used as a phytotherapeutic agent for cardiovascular, metabolic, immune, nervous, and reproductive health. In this study, a multidisciplinary approach combining nutrigenomic analyses, cardiovascular physiology experiments, and phytochemical and ethnobotanical data was employed to investigate the effects of aqueous extract (ZLex). ZLex significantly upregulated genes involved in nitric oxide synthesis (, ), smooth muscle relaxation, and angiotensin degradation, correlating with reductions in systolic, diastolic, and mean arterial blood pressure. In addition, ZLex modulated key neurotransmission-related genes (, , ), supporting its potential anxiolytic and neuroprotective actions. Immune modulation was indicated by the upregulation of genes associated with anti-inflammatory and antimicrobial responses. Metabolic benefits were linked to the regulation of genes involved in glucose and lipid metabolism, mitochondrial function, and body weight control. Positive effects on reproductive health were suggested by the induction of genes implicated in spermatogenesis. These effects are likely mediated by bioactive constituents such as rutin, kaempferol-3-O-rutinoside, 3',5'-di-C-β-glucopyranosylphloretin, a quercetin dirhamnosyl-galactoside, and myricetin-3-O-rutinoside. Altogether, the findings provide mechanistic support for the traditional use of and highlight its therapeutic potential in managing hypertension and other chronic disorders, including diabetes, obesity, and anxiety. - Source: PubMed
Publication date: 2026/03/04
Alla ChaimaeLucau-Danila AncaMehiou AfafAkissi Zachee L EHilbert Jean-LouisLegssyer AbdelkhaleqSahpaz SevserZiyyat Abderrahim - We investigated the correlation between increased gene copy number of gamma aminobutyric acid type A (GABA) receptor α5-containing subunits and electrophysiological and behavioral phenotypes in a mouse model of Dup15q syndrome (15q dup) and tested the hypothesis that selectively inhibiting the activity of GABA-α5 receptors may have therapeutic effects. Dup15q syndrome is a rare neurodevelopmental disorder caused by copy number gains of the 15q11.2-q13.1 chromosomal region, which includes UBE3A and a cluster of three genes (GABRA5, GABRB3, and GABRG3) encoding GABA receptor subunits, all of which are critical for neural development and function. Most affected children display hypotonia, motor delays, intellectual disability, and epilepsy, as well as a characteristic electroencephalography (EEG) beta-band phenotype. There is no disease-modifying therapy available. Autoradiography showed increased density of GABA-α5 receptors in the brains of 15q dup mice, while electrophysiology revealed enhanced GABAergic transmission in hippocampal slices from these mice. A GABA-α5 negative allosteric modulator, RO4938581, decreased inhibitory synaptic charge transfer in 15q dup hippocampal slices. The behavioral analyses confirmed inflexibility in learning and abnormal social behaviors in 15q dup mice, and both phenotypes were normalized following chronic treatment with RO4938581. EEG recordings showed increased beta-power in 15q dup mice - which resembled the spectral signature of subjects with Dup15q - and was partially normalized following RO4938581 treatment. Our results suggest that excessive expression and function of the GABA-α5 receptor subtype plays a key role in the pathophysiology of Dup15q and GABA-α5 NAMs may represent a potential precision medicine therapeutic option. - Source: PubMed
Publication date: 2026/01/05
Nakagawa RyokoNani FrancescaHipp Joerg FHoner MichaelKnoflach FredericGasser RodolfoOzmen LaurenceTamada KotaFjeldskaar FatihaTakacs LiviaVautheny AudreyMorairty Stephen RSaxe MichaelTakumi ToruHernandez Maria-Clemencia - Egg components, including weight of yolk, albumen, and eggshell, are economically important traits in poultry breeding and production, and we thus conducted a genome-wide association study (GWAS) for them. We used an F resource population of hens ( = 142) in different periods of laying, obtained by crossing breeds with contrasting phenotypes, and then genotyped them using the Illumina Chicken 60K iSelect BeadChip. Significant associations were found between 33 single nucleotide polymorphisms (SNPs) and yolk weight at 18-28 weeks of age (YW1). Eighty-seven SNPs were associated with thick albumen weight at 18-28 (TAW1) and 29-42 (TAW2) weeks of age. Four SNPs were associated with eggshell weight at 18-28 weeks of age (ESW1). Fifty-three candidate genes were identified in the positions of these SNPs, and seven prioritized candidate genes (PGCs) were revealed in regions where 2-4 SNPs associated with the studied traits were localized. These were as follows: (YW1, TAW1), (TAW1), (YW1, TAW1), (YW1), (YW1), (YW1), and (TAW1). Allelic variants at the , , , and loci were associated with higher YW1 and TAW1. These SNPs and PGCs are potential genetic markers for characterizing egg weight parameters and their components in chicken breeding to achieve egg production improvements. - Source: PubMed
Publication date: 2025/11/24
Volkova Natalia ARomanov Michael NLarionova Polina VDzhagaev Alan YuVolkova Ludmila ASermyagin Alexander AGriffin Darren KZinovieva Natalia A - Given the emerging understanding of neurotransmitter involvement in cancer biology, GABA receptors have garnered attention for their diverse and sometimes controversial roles across cancer types. Hence, this study aimed to investigate the expression patterns of GABA-A receptors in glioblastoma, breast, and ovarian cancer cells and their impact on cellular responses via an agonist‒antagonist approach. Cell proliferation and cytotoxicity were assessed using MTT and AO/PI assays, respectively. GABA treatment significantly influenced proliferation, stimulating it in ovarian A2780CP cells overexpressing GABRG3 and inhibiting it in U87 glioblastoma cells, which showed increased expression of GABRR3. Furthermore, GABA reduced CD133+ and CD44+ stem-like populations in A2780CP cells and decreased the CD44+ fraction in MDA-MB231 cells, correlating with specific GABA-A receptor subunit expression. Migration assays revealed that GABA significantly reduced the motility of MDA-MB231 and MCF-7 cells, possibly through modulation of GABRR2 expression. EMT-related transcription factors and markers were evaluated using qPCR, flow cytometry, and Western blot analysis. Protein-level changes in EMT markers confirmed the transcriptional data, with GABA modulating E-cadherin and Vimentin expression in a cell-specific manner. These findings underscore the critical role of GABA-A receptor subtypes in promoting or suppressing cancer progression through context-dependent regulation of proliferation, stemness, migration, and EMT. - Source: PubMed
Publication date: 2025/09/29
Khodaei MaryamHosseinmardi NargesSirati-Sabet MajidSahranavard ShamimShahmohammadi Mohammad RezaSalami Siamak