Adcy3
- Known as:
- Adcy3
- Catalog number:
- 038210A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Adcy3
Related genes to: Adcy3
- Gene:
- ADCY3 NIH gene
- Name:
- adenylate cyclase 3
- Previous symbol:
- -
- Synonyms:
- AC3
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-22
- Date modifiied:
- 2015-08-26
Related products to: Adcy3
Related articles to: Adcy3
- Non-syndromic monogenic obesity, caused by defects in the leptin-melanocortin pathway, presents with early-onset severe obesity and hyperphagia, but genotype-phenotype and metabolic correlations across different genetic forms remain unclear. - Source: PubMed
Kahveci AhmetKarauzum Selin UzunManyas HayrullahOzdemir Behiye SarikayaOrbak ZerrinTercan UmmahanYildirim RukenHatipoglu NihalKilci FatihNursoy HaticeOzalkak ServanKolbasi BarisCetinkaya SemraOzdemir Hazal CanbazParlak MesutKokenli Filiz TutunculerCamtosun EmineDibeklioglu Saime ErgenBuyukyilmaz GonulBulus Ayse DeryaBalki Hanife GulOzden AyseGonc E NazliOzsu ElifDemirbilek HuseyinYildiz MelekOzen SamimBereket AbdullahHaliloglu Belma - Olfactory stimulation has emerged as a non-invasive strategy to modulate brain function; however, the molecular mechanisms linking odorant-receptor interactions to central neurobiological outcomes remain poorly defined. In this study, we investigated the antidepressant-like effects of linalyl acetate (LA) and elucidated its olfactory-driven signaling mechanisms using integrated computational, transcriptomic, and in vivo approaches. In silico analyses identified OR2B3 as a candidate olfactory receptor for LA, supported by structural similarity assessment and docking simulations. In human nasal epithelial cells, LA treatment induced coordinated transcriptional programs enriched for olfactory receptors, chemosensory cilia, GPCR signaling, and synapse-related pathways, indicating activation of receptor-guided sensory signaling networks. These findings were further supported by RT-PCR validation, which confirmed significant upregulation of OR2B3 and OR6A2, as well as modulation of cilium-associated signaling components, including ADCY3. In vivo, repeated LA inhalation significantly reduced immobility time in the tail suspension test, demonstrating antidepressant-like behavioral effects. These behavioral outcomes were accompanied by decreased serum corticosterone and pro-inflammatory cytokines, together with increased brain-derived neurotrophic factor levels in serum, cerebral cortex, and hippocampus. Neurochemical analyses further revealed enhanced monoaminergic (dopamine, noradrenaline, serotonin) and cholinergic signaling. Transcriptomic profiling of the olfactory bulb and hippocampus revealed dose-dependent enrichment of metabolic, synaptic, neurotrophin, and intracellular signaling pathways, highlighting coordinated metabolic-synaptic coupling and neuroplasticity-associated programs. Collectively, these findings demonstrate that LA engages olfactory receptors to activate cilia-centered chemosensory signaling that propagates into central metabolic, synaptic, and neurotrophic networks, ultimately modulating stress-related neurobiology. This study establishes a molecular framework for odorant-mediated neuromodulation and supports the therapeutic potential of olfactory-based interventions for mood regulation. - Source: PubMed
Publication date: 2026/04/30
Ferdousi FarhanaSasaki KazunoriNakai ToshiakiNiki AikoNakajima MitsutoshiIsoda Hiroko - Genome-wide association studies (GWASs) have identified hundreds of obesity-associated SNPs, but establishing their causality remains challenging. Here, we demonstrate that rs11676272, located in the ADCY3 gene, is a functional causal variant for obesity susceptibility. Bioinformatic analyses and dual-luciferase reporter assays indicate that the rs11676272 region may act as a human-gained enhancer regulating ADCY3 expression. In HEK293T cells, CRISPR-Cas9-mediated single-nucleotide editing of rs11676272 (T > C) reduces ADCY3 expression. Moreover, the rs11676272-T allele is preferentially bound by the transcription factor E2F3 to upregulate ADCY3 expression, whereas the rs11676272-C risk allele loses this binding. In vivo, the rs11676272 T > C variant in human ADCY3 (hADCY3) knock-in mice accelerates weight gain under high-fat diet conditions and shortens primary cilia in the ventromedial hypothalamus (VMH). CRISPRa-mediated activation of the hADCY3 promoter region rescues ciliary length in both the VMH and hypothalamic arcuate nucleus of Mut-hADCY3 mice. Our data reveal a causal role for rs11676272 in obesity, offering insight into potential therapeutic strategies. - Source: PubMed
Publication date: 2026/04/06
Wang WeinaLi YueDong ShengLiu YuweiGuo ChenghangSu YuzheTian WeiHu XiaoyuWang Zhenshan - Breast cancer is a common malignant tumor with a complex pathogenesis, and while genome-wide association studies (GWAS) have identified multiple risk loci, they often fall short in pinpointing specific functional susceptibility genes. To address this, we collected whole-tissue eQTL data from the GTEx portal and breast cancer GWAS summary data from the Breast Cancer Association Consortium (BCAC) and FinnGen R10 database, employing transcriptome-wide association studies (TWAS) to screen and identify susceptibility genes. Subsequently, spatial transcriptomic sequencing and single-cell RNA sequencing were employed to investigate the underlying mechanisms of these genes within the tumor microenvironment (TME) and their relevance as therapeutic targets. We identified five susceptibility genes-ADCY3, CASP8, GRHL1, HELQ, and TLR1-which are enriched in tumor-related signaling pathways such as Kras and TNFα. In the breast cancer TME, these genes are associated with myofibroblasts, mast cells, and M2 macrophages, and these cells may interact via biological pathways involving macrophage migration inhibitory factor (MIF) and secreted phosphoprotein 1 (SPP1). Notably, TLR1 may serve as a drug target, with compounds such as Doxorubicin and Etoposide identified as potential candidates. In conclusion, ADCY3, CASP8, GRHL1, HELQ, and TLR1, as genetic susceptibility genes for breast cancer, hold significant value in understanding tumor development and advancing therapy. - Source: PubMed
Publication date: 2026/02/17
Zhang JingmeiChen Zhiting - Modern lifestyles often disturb circadian rhythms, yet the genetic circuits that convert this stress into metabolic dysfunction remain poorly defined. Here, we identify a missense variant in (rs11676272; Ser107Pro) as a pleiotropic regulator of circadian preference and adiposity. Using genome-wide pleiotropy analysis in ∼480,000 UK Biobank participants, we show that the G risk allele (Pro107) increases eveningness, BMI, and fat mass in European ( = 451,324) and African ( = 8,738) ancestry groups, with behavioral amplification by morning difficulty awakening in Europeans and power-limited modeling in other populations. Structural modeling and transcriptomic analysis suggest this allele alters adipose-specific splicing and expression and destabilizes ADCY3 protein. In mice, is rhythmically expressed in adipose tissue, with BMAL1 binding near the orthologous residue 107 site. Human adipose expression also increases after weight loss. Together, these findings reveal a genotype-dependent, behaviorally modifiable axis connecting difficulty awakening to metabolic risk through circadian and adipose regulatory pathways. - Source: PubMed
Publication date: 2025/12/30
Tchio CynthiaMaher MatthewMoth ChristopherMeiler JensLane Jacqueline MTaylor Herman AWilliams Jonathan SSaxena Richa