GABBR2 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- GABBR2 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb127371
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- GABBR2 antibody Polyclonal Antibodies Primary antibodies
Related genes to: GABBR2 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- GABBR2 NIH gene
- Name:
- gamma-aminobutyric acid type B receptor subunit 2
- Previous symbol:
- GPR51
- Synonyms:
- HG20, GABABR2, GPRC3B
- Chromosome:
- 9q22.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-23
- Date modifiied:
- 2016-10-05
Related products to: GABBR2 antibody Polyclonal Antibodies Primary antibodies
Related articles to: GABBR2 antibody Polyclonal Antibodies Primary antibodies
- Autism spectrum disorder (ASD) is a multifactorial neurodevelopmental disorder with complex molecular etiology. Since genetic causes account for less than 50% of ASD cases, novel approaches are required to overcome the challenges of characterizing genes and molecular pathways linking risk alleles to phenotype. Here we use RNA-sequencing, 3-dimensional protein-centric chromatin conformation (Hi-ChIP), and whole genome DNA methylation sequencing approaches to investigate hippocampal tissue from an ASD mouse model (Cntnap2 knockout [Cntnap2 KO]) to determine if multi-omic data integration improves the resolution of key molecular pathways contributing to the complex ASD phenotype. Each -omic dataset individually identified disruptions in numerous genes and pathways, providing broad ASD-related insights, such as 1) 699 downregulated genes with an enrichment of neuronal ontological terms; 2) unique chromatin interactions in Cntnap2 KO mice; and 3) that most differentially methylated genes (1220/1659) have a neuronal function. The multi-omic data integration reduced the heterogeneity and refined the data to 43 genes with links to ASD (e.g., Zbtb18, Cttnbp2, Gabbr2). A pathways analysis of these 43 genes identified one gene ontological term: regulation of neuronal synaptic plasticity. These findings are consistent with large scale gene expression studies of human ASD postmortem brain tissue, suggesting that multi-omic data integration can be used to achieve a greater resolution of the heterogeneous ASD molecular etiology. - Source: PubMed
Publication date: 2026/07/25
Alberca Carolina DPark KwangmoonPapale Ligia AMadrid AndyBergmann Phillip EKeleş SündüzAlisch Reid S - Exercise-induced regulation of cortical GPCR pathways in diabetic obesity remains unclear. This study aimed to investigate exercise-associated GPCR-related transcriptomic pathway changes in the cerebral cortex of diabetic-obese rats. Cerebral cortical samples from male Zucker Fatty Diabetes Mellitus (ZFDM) rats subjected to a 12-week swimming program were examined using RNA sequencing, functional enrichment, GSOAP clustering, and STRING-based protein-protein interaction (PPI) analysis. Exercise training reduced fasting glucose and body weight. RNA sequencing identified 817 exercise-responsive transcripts (403 upregulated and 414 downregulated; < 0.05), including 48 associated with GPCR signaling. Results showed that these 48 genes mapped to three major GPCR-related networks: cAMP signaling, with increased Adcyap1r1, Gipr, Tshr, and Vipr2 and decreased Vip, Chrm1, Gabbr2, and Sst; calcium signaling, with increased Ntsr1 and Trhr and decreased Chrm1; and neuroactive ligand-receptor interaction, with increased Trh, Trhr, and Crh and decreased Opr-related transcripts. These findings provide hypothesis-generating evidence for interpreting cortical GPCR-related transcriptomic pathway associations in diabetic-obese conditions. - Source: PubMed
Publication date: 2026/06/21
Chiang Yin-YuWidjaya Michael AneksonLee Shin-Da - Certain events that occur in early life, such as changes in nutrition, can induce structural and functional modifications in brain development, leading to behavioral programing in the offspring. These effects depend on the timing, intensity, and duration of exposure, and may contribute to chronic disorders in adulthood. Artificial non-nutritive sweeteners (NNS), such as saccharin, have recently been proposed as potential developmental disruptors. Saccharin consumption during pregnancy is discouraged, as it can cross the placenta and accumulate in the fetus. - Source: PubMed
Publication date: 2026/04/30
Pacheco-Sánchez BeatrizLópez-Merchán RaquelRubio PabloGarcía-Martos PilarSuárez JuanSanjuan CarlosRubio LeticiaMartín-de-Las-Heras StellaRodríguez de Fonseca FernandoAlén Franciscode Ceglia MarialuisaRivera Patricia - Context-induced relapse is a significant factor limiting recovery from alcohol use disorder (AUD). However, the molecular processes in the hippocampus, critical for contextual memory, impacted by chronic alcohol use, remain poorly understood. We used a non-human primate model to test the hypothesis that chronic alcohol use impacts hippocampal molecular pathways that may serve as therapeutic targets for memory processing in chronic alcohol use. We conducted RNAseq profiling on hippocampal samples from adult male rhesus monkeys with chronic alcohol use (n = 7) and controls (n = 5). We identified 2,575 differentially expressed genes in subjects with chronic alcohol use, including genes implicated in genome-wide association studies of alcohol dependence, such as GLP2R and GABBR2. Downregulated pathways included chemical synaptic transmission, trans-synaptic signaling, and neuron development, and upregulated pathways involved mitochondrial function. Targeted pathway analysis highlighted downregulation of synaptic signaling and upregulation of mitochondrial processes. Leading-edge gene analysis revealed downregulated genes involved in synaptic signaling and upregulated genes involved in mitochondrial processes. Drug repurposing analysis identified several potential therapeutic targets, including epidermal growth factor receptor inhibitors and L-type calcium channel blockers. Our results provide critical insights into molecular pathways underlying hippocampal pathology in chronic alcohol use and offer potential novel therapeutic targets. - Source: PubMed
Publication date: 2026/05/06
Pareek TanyaVergis John MZhang XiaoluPlatt Donna MGrant Kathleen AMcCullumsmith RobertGisabella BarbaraO'Donovan Sinead MPantazopoulos Harry - BACKGROUND: Autism spectrum disorder (ASD) shows a consistent sex bias, yet how sex shapes de novo variant (DNV) risk across coding and noncoding sequence remains unclear. I analyzed DNVs in > 41,000 parent–child sequenced trios from three ASD family-based cohorts and compared DNV characteristics and enrichment patterns in males and females. Notably, these trios included individuals with ASD as well as those without ASD. I developed a new sex-aware DNV caller (HAT-FLEX) and thoroughly evaluated each candidate DNV using an additional tool introduced in this study, SNOW, to generate a high-confidence callset. RESULTS: I identified enrichment of missense and loss-of-function (LOF) DNVs both overall and within known ASD-related genes (i.e., SFARI genes). Gene-specific enrichment analyses revealed twelve genes that were exome-wide significant and specific to males, for significance, including FOXP1, SMAD6, AUTS2, CCDC168, PIEZO1, EML6, ZNF84, IGSF23, OTOG, NHSL1, ADNP, and FREM3 and three genes that were specific to females, for significance, including TAOK1, MECP2, and DDX3X within a variant class. Direct comparisons of DNVs in males and females revealed MECP2 as the only exome-wide significant gene; however, GABBR2 was also trending toward enrichment in the direct males with ASD comparison to females with ASD. Furthermore, probit analyses support a female protective effect and demonstrates that damaging DNVs, particularly LOF variants, including potentially stronger X-linked effects in females, are associated with increased ASD liability, whereas synonymous variants are not. Finally, I analyzed promoters and identified a single significant promoter region (p = 3.8 × 10−13), associated with the WDR74 gene, with the signal driven by DNVs observed in males with ASD. Surprisingly, the noncoding RNA gene RNU2-2 lies within this significant WDR74 promoter and accounted for most of the DNVs in the region. RNU2-2 DNVs were present in 0.2% of individuals with ASD in comparison to 0.05% of individuals without ASD. CONCLUSIONS: These findings show that ASD DNV risk differs by sex at both the gene and liability levels, supporting a female protective effect while highlighting sex-specific patterns in coding variation. They also identify RNU2-2 as a noncoding contributor to ASD risk, expanding the landscape of ASD-associated variation beyond protein-coding genes. - Source: PubMed
Publication date: 2026/04/24
Turner Tychele N