GNAT3 antibody
- Known as:
- GNAT3 (anti-)
- Catalog number:
- orb101872
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- GNAT3 antibody
Related genes to: GNAT3 antibody
- Gene:
- GNAT3 NIH gene
- Name:
- G protein subunit alpha transducin 3
- Previous symbol:
- -
- Synonyms:
- gustducin, GDCA
- Chromosome:
- 7q21.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-29
- Date modifiied:
- 2018-11-15
Related products to: GNAT3 antibody
Related articles to: GNAT3 antibody
- Taste receptors, including bitter (TAS2Rs), sweet (TAS1R2/TAS1R3), and umami (TAS1R1/TAS1R3) receptors, have recently attracted attention in cancer research due to their emerging relevance in tumour biology. Glioblastoma is the most common and aggressive primary brain tumour, yet its chemosensory properties remain poorly characterised and taste receptor expression has not previously been investigated in this type of cancer. Here, we performed a comprehensive characterisation of taste receptor expression in glioblastoma using human astrocytes, three glioblastoma cell lines, and human tumour samples. Transcript analysis identified 20 of the 26 human TAS2Rs, as well as TAS1R2/TAS1R3 and TAS1R1/TAS1R3, in glioblastoma cell lines. Selected receptors (TAS2R4, TAS2R5, TAS2R14, TAS2R39, and TAS1R2/TAS1R3) were further examined at the protein level by Western blot and immunocytochemistry, confirming their presence across the tested models. Immunohistochemistry in tumour samples from 13 glioblastoma patients demonstrated variable receptor expression, revealing receptor-specific distribution patterns within tumour tissue. In addition, the taste-signalling protein GNAT3 was detected in glioblastoma cells, supporting the presence of the taste pathway components. Together, these findings provide the first transcript and protein-level mapping of taste receptors in glioblastoma, establishing a molecular atlas of these chemosensory receptors in cell models and human tumours. This work lays a foundation for future studies investigating the biological significance of taste receptors in glioblastoma. - Source: PubMed
Publication date: 2026/05/07
Costa Ana RFerreira Catarina LBessa-Soares TâniaDuarte Ana CGonçalves IsabelCavaco J EduardoFerrer IsidroFurihata TomomiMarcelino HelenaCascalheira José FSantos Cecília R A - Bitter taste receptors (TAS2Rs) are increasingly recognised as extraoral chemosensors that modulate diverse biological processes, including cancer cell behaviour and drug responsiveness. Many TAS2R ligands correspond to therapeutic compounds; however, their contribution to the response of brain tumours to chemotherapy remains unexplored. Here, we investigated whether the bitter taste signalling pathway is modulated by temozolomide (TMZ), the standard chemotherapeutic agent for glioblastoma, with an impact on treatment efficacy in glioblastoma cells. We show that TMZ elicits intracellular Ca responses compatible with activation of G-protein-coupled receptor signalling and induces anti-proliferative and pro-apoptotic effects in multiple human glioblastoma cell lines. Pharmacological inhibition of bitter taste receptors, as well as genetic silencing of the taste transduction G protein GNAT3, significantly attenuated TMZ-induced cytotoxicity, suggesting that bitter taste signalling is involved in this process. In silico ligand prediction combined with receptor expression profiling identified TAS2R43 as a candidate modulator of these effects, and TAS2R43 knockdown markedly reduced TMZ-induced loss of cell viability and apoptosis. Moreover, TMZ enhanced intracellular accumulation of the ABC transporter substrate doxorubicin, suggesting modulation of multidrug efflux mechanisms. Collectively, our findings identify TAS2R43 as a potential biomarker that warrants further validation to improve responses to TMZ and other ABC transporter-limited anticancer drugs. - Source: PubMed
Publication date: 2026/04/03
Costa Ana RDuarte Ana CGonçalves IsabelPreissner RobertCascalheira José FMarcelino HelenaSantos Cecília R A - Chemosensory cell clusters are taste bud-like sensory structures located in the pharyngo-laryngeal mucosa. These clusters are densely distributed at the entrance of lower airways to detect chemical stimuli and trigger respiratory reflexes; however, their postnatal development remains poorly understood. In this study, we examined postnatal changes in the morphology and distribution of chemosensory clusters in rat laryngeal whole-mount preparations using immunofluorescence for alpha-gustducin (GNAT3, a marker of type II taste cells) and synaptotagmin-1 (Syt1, a marker of type III taste cells). Chemosensory cell clusters were detected along the margin of the epiglottis on postnatal day 2 (PD2). Their numbers rapidly increased by PD7 (26 ± 4.5) and plateaued by postnatal week 3 (PW3, 84.0 ± 4.9), whereas the number of constituent cells continued to increase until PW8. Clusters at early stages (PD2-PD7) contained 2-3 spindle GNAT3-immunoreactive cells and round Syt1-immunoreactive cells. As the cluster matured, both cell types elongated longitudinally, extended the apical tip of their cytoplasmic processes to the epithelial surface, and GNAT3-immunoreactive cells developed branched cytoplasmic processes. P2X3-immunoreactive afferent nerve endings contacted GNAT3- and Syt1-immunoreactive cells throughout development. The results indicate the constant presence of chemosensory cell clusters in the laryngeal entrance and the establishment of neuronal connections as early as PD2. These clusters may be sentinel chemoreceptors at the entrance of the larynx. Because stabilization of chemosensory cell cluster numbers coincides with the weaning period, the postnatal development of these clusters may be associated with feeding behaviors in rats. - Source: PubMed
Publication date: 2026/02/26
Abdali Sayed SharifMiyazaki KannaYokoyama TakuyaNakamuta NobuakiSaino TomoyukiYamamoto Yoshio - This study evaluates and compares the protective effects of several type II taste receptor (T2R) agonists against LPS (lipopolysaccharide)-induced inflammatory damage in BEAS-2B cells, focusing on their action via an α-gustducin (encoded by )-dependent signaling pathway that leads to NF-κB inhibition. To investigate gene expression, mRNA levels of target inflammatory cytokines and T2R subtypes were quantified by qRT-PCR. Cytotoxicity assessment of LPS and bitter agonists was conducted using the CCK-8 assay. The activation status of the NF-κB pathway was examined by Western blot analysis of total and phosphorylated forms of p65 and IκB. Finally, the specific and essential role of GNAT3 was definitively validated through siRNA-mediated gene knockdown. LPS treatment induced significant upregulation of IL-6 and IL-8 mRNA, along with increased phosphorylation of p65 and IκB in BEAS-2B cells. A direct, parallel comparison of the bitter taste agonists PTC (phenylthiourea), QN (quinine), CPD (carisoprodol), and LK (chloroquine) revealed their capacity to upregulate specific T2R subtypes, suppressing inflammatory mediator release and NF-κB activation. Critically, upon silencing, the inhibitory effects of all tested agonists on p-p65/p65 and p-IκB/IκB ratios were significantly attenuated, without altering total p65 or IκB abundance. This provides direct genetic evidence that GNAT3 is specifically required for mediating the anti-inflammatory effects elicited by these T2R agonists. Multiple bitter receptor agonists exert anti-inflammatory effects on airway epithelial cells in a GNAT3-dependent manner. Our study advances the field by systematically comparing agonist efficacy and establishing the indispensable role of GNAT3 within the anti-inflammatory signaling cascade triggered by T2R agonists, thereby revealing a refined mechanistic insight and potential therapeutic target for inflammatory lung diseases. - Source: PubMed
Publication date: 2026/01/19
Fang YuzhenWang QiujieWu ShuobinHe XinxiuWang ShengyuMa RuonanZhao HaoZhao XiaoyiWang XingZhang Yuxin - Bitter taste receptors (TAS2Rs), initially identified for chemosensory roles in the tongue, are expressed in extraoral tissues, including the airways. However, to date, it remains unclear whether bitter signaling is associated with susceptibility to bacterial infection in the lower airways and whether bitter signaling actually participates in the immune response in lung infection has yet to be genetically established. Here, we investigated the role of TAS2R signaling in -induced murine pneumonia via wild-type (WT) and several mutants (mTas2r104/105, mTas2r105/114, mTas2r104/105/114, Gnat3 and Gnat3mTas2r104/105) mice. Genetic disruption of TAS2Rs altered compensatory expression of other bitter receptors in the trachea and lungs, but did not affect immune cell composition in the lungs or thymus. Bitter receptor-deficient mice exhibited exacerbated pulmonary lesions at day 3 (D3) post-infection. Pulmonary infection significantly upregulated ,, , , , , and in the lung. TAS2R signaling deficiency downregulated the expression of cytokines (e.g., IL-10, MIP-2) and antimicrobial peptides in the lungs and trachea, increased CD68+ macrophages in D3 lung tissues, amplified Ki67+ cell proliferation in alveolar and bronchiolar regions, and even impaired recovery from lung injury by day 14 (D14). Mechanistically, bitter taste pathway disruption dysregulated the mTOR pathway, reduced eNOS expression, and delayed resolution of pneumonia-induced injury. In summary, the current results collectively indicate that bitter taste signaling can modulate innate immune and inflammatory responses during S. aureus-induced lung infection. - Source: PubMed
Publication date: 2025/10/09
Liu Ling-LingLi FengZhu Meng-MinNiu Bo-WenHuang YuChen LixiangYang HuaQin BoyinZhou Xiaohui