Ask about this productRelated genes to: GABRA2 Blocking Peptide
- Gene:
- GABRA2 NIH gene
- Name:
- gamma-aminobutyric acid type A receptor alpha2 subunit
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4p12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-02
- Date modifiied:
- 2016-02-04
Related products to: GABRA2 Blocking Peptide
Related articles to: GABRA2 Blocking Peptide
- Alcohol use disorder (AUD) is influenced by genetic factors that affect key neurobiological systems, including dopaminergic and GABAergic pathways, which regulate neurobehavioral functions and are modulated by brain-derived neurotrophic factor (BDNF). Variations in these genes contribute to individual vulnerability to AUD. In this study, we investigated single-nucleotide polymorphisms (SNPs) and haplotypic associations in , , and , along with the dopaminergic pathway genes / and , in a Spanish cohort. Peripheral blood-derived genomic DNA was genotyped, and haplotype analyses were conducted. Individual SNPs in , , BDNF, and / showed no significant associations with AUD. In , the rs3219151 T allele was more frequent in AUD patients than in controls (57.9% vs. 49.3%; = 0.03), while the C allele appeared to show a potential protective association. In addition, the GAC haplotype of (rs2197414, rs1992647, rs3219151) was less frequent in AUD than in controls (0.071 vs. 0.122) and showed a protective association (OR = 0.58; 95% CI = 0.34-0.99; = 0.045). Our findings provide exploratory evidence suggesting that specific genetic variants and haplotypes may contribute to AUD susceptibility and support the relevance of multigenic and haplotypic approaches for exploring the neurobiological mechanisms underlying AUD. - Source: PubMed
Publication date: 2026/06/15
Rojas-Pirela MauraGómez Lesmes Sandra PatriciaSalete-Granado DanielLlorente HernánPérez Nieto María-ÁngelesNovo-Veleiro IgnacioCieza-Borrella ClaraPastor IsabelFernández-Mateos JavierInés Revuelta Sandra MChamorro Antonio-JavierLaso Francisco-JavierGonzález-Sarmiento RogelioMarcos Miguel - Gene-environment interactions are thought to contribute to neurodevelopmental psychiatric disorders, yet their behavioral and molecular consequences remain incompletely understood. Here, we examined whether partial deficiency of reelin (Reln) increases susceptibility to a mild prenatal immune challenge in mice. Heterozygous Reln mice and wild-type littermates were exposed to low-dose polyinosinic-polycytidylic acid (Poly(I:C); 2 mg/kg, intraperitoneally) at embryonic day 12.5. Adult male offspring were assessed in the open-field, three-chamber social interaction, and marble-burying tests, followed by gene expression analysis in the medial prefrontal cortex (mPFC). In the open-field test, prenatal Poly(I:C) exposure was associated with increased locomotor activity during the late habituation phase, with the clearest increase in the combined-risk group. In the social interaction test, significant social novelty preference was not detected in the combined-risk group, whereas sociability toward an unfamiliar conspecific was preserved across groups. Marble-burying behavior was reduced in heterozygous Reln mice irrespective of immune challenge, suggesting a genotype-related behavioral alteration that was partly distinct from the combined-risk phenotype observed in the other tests. In the mPFC, several γ-aminobutyric acid A (GABA) receptor subunit transcripts were altered in a gene- and exposure-specific manner. Gabra2 expression was reduced in the combined-risk group, whereas Reln expression was decreased in heterozygous mice independent of immune challenge. These findings indicate that partial Reln deficiency provides a permissive genetic background in which mild prenatal immune activation subtly alters higher-order behavioral adaptation and prefrontal GABA-related gene expression. - Source: PubMed
Iwata KeikoShintani NorihitoMatsuzaki Hideo - The central nervous system responds to acute injury with plastic remodeling of its network. However, the temporal and structural dynamics of this response in the denervated dentate gyrus remain poorly understood. Therefore, we examined the transcriptional programs activated after perforant path transection, focusing on the outer molecular layer (OML) and the granule cell layer (GCL). - Source: PubMed
Publication date: 2026/05/19
Schlaudraff JessicaDel Turco DomenicoKey JanaDeller ThomasAuburger Georg - The RNA helicase MOV10 is highly expressed in developing brain, is present in synapses and is required for embryonic viability. A murine brain-specific knockout of MOV10 ( Deletion) has a thickened cortex, abnormal dendritic arborization and enhanced fear memory. In human studies, is among the loci that is correlated with enhanced cortical brain volumes and is also significantly associated with substance dependence by epigenetic profiling. Here we demonstrate that Deletion mice show enhanced fear learning that is aligned with impaired structural connectivity of canonical fear circuits revealed by Diffusion Tensor Imaging. We propose a model where MOV10 loss leads to increased GABRA2 expression in the hippocampus and reduced anatomical connectivity that drives augmented fear learning. Memory reactivation is observable during fear memory retrieval as an overall increase in fMRI functional activity in cortical regions. Taken together, this framework identifies that enhanced fear in the MOV10 model is driven via a "corticalized" fear response during re-exposure to the training context that is not driven by the canonical fear circuit. These findings support a molecular basis for non-traditional enhanced learning mechanisms activated by fearful events that shed light on the intractability of fear memories with the potential to inform PTSD and substance dependence disorders. - Source: PubMed
Publication date: 2026/05/18
Shilikbay TemirlanNawaz AatiqaSun MenghanDoon MeganOlmo IsabellaCumbie LeoBenson JuliusIbrahim BaherTsai Nien-PeiLlano DanielGoense JozienGritton HowardCeman Stephanie - Diethylene glycol dibenzoate (DEGDB), an emerging eco-friendly plasticizer, remains critically understudied with mechanistic and molecular-level evidence linking it to clear cell renal cell carcinoma (ccRCC) progression, representing a major knowledge gap. To fill this gap, we conducted a cross-scale investigation using network toxicology, WGCNA, machine learning, SHAP explainable modeling, and molecular docking as methodological tools to elucidate DEGDB‑induced ccRCC progression. By jointly mining the ChEMBL, PubChem, SwissADME, STRING, and GEO repositories, we rigorously distilled a high-confidence set of 42 target genes, among which TSHR, ADORA2B, ANPEP, CA9, CYP3A4, JUN, NR1I3, and PHGDH were highlighted. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses revealed that DEGDB may propel ccRCC progression by disrupting neuro-endocrine-immune network regulation, activating chemical carcinogenesis-related receptors, and perturbing metabolic-degradation pathways such as nitrogen metabolism and lysosomal signaling. Subsequently, 113 machine-learning algorithms were leveraged to construct predictive models, and SHAP-based interpretation pinpointed five core genes-CA9, NR1I3, PHGDH, GABRA2, and ANPEP. Validation against The Cancer Genome Atlas (TCGA) datasets demonstrated that CA9 exhibits marked expression divergence in ccRCC (box-plot analysis) and is strongly associated with unfavorable prognosis (Kaplan-Meier survival curves). Molecular-docking simulations further confirmed robust binding affinities between DEGDB and all five core target proteins (binding energies < -5 kcal/mol). In vitro assays additionally revealed that DEGDB significantly promotes 786-O and A498 proliferation and up-regulates CA9 protein expression. Collectively, our findings indicate that DEGDB accelerates ccRCC progression via the orchestrated modulation of cellular proliferation, disruption of neuro-endocrine-immune homeostasis, and activation of oncogenic receptors. This study provides a theoretical framework for assessing the environmentally relevant health risks posed by emerging plasticizers and for devising preventive strategies against DEGDB‑induced ccRCC under real‑world exposure scenarios. - Source: PubMed
Publication date: 2026/05/22
Yanping MaGuolin TianTao YangAngyang DuJiaxin LiBo TaoYajie LiYaodong JiaYuelong FengHao YangLihong NieRuining Zhao