GNAO1 Antibody (OALA03458)
- Known as:
- GNAO1 Antibody (OALA03458)
- Catalog number:
- oala03458
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GNAO1 Antibody (OALA03458)
Related genes to: GNAO1 Antibody (OALA03458)
- Gene:
- GNAO1 NIH gene
- Name:
- G protein subunit alpha o1
- Previous symbol:
- -
- Synonyms:
- G-ALPHA-o
- Chromosome:
- 16q13
- Locus Type:
- gene with protein product
- Date approved:
- 1988-04-24
- Date modifiied:
- 2016-03-03
Related products to: GNAO1 Antibody (OALA03458)
Related articles to: GNAO1 Antibody (OALA03458)
- Stem cell proliferation rates must be precisely regulated as insufficient proliferation leads to tissue loss, whereas excessive proliferation causes tumorigenesis and cancer. A homeostatic balance is therefore achieved through feedback loops that adjust stem/progenitor cell proliferation rates to match the demand for their differentiated progeny. While such a homeostatic feedback mechanism adjusts germline stem cell (GSC) proliferation rates to oocyte needs in the adult hermaphrodite germline, its inner workings are incompletely understood. Here we show that the Gα GOA-1 /GNAO1 is required specifically in the gonadal sheath cells to non-autonomously promote GSC quiescence in spermless hermaphrodites. Given that dysregulation of G protein signalling is frequently observed in human cancers, Gα dependent homeostatic control of stem cell proliferation may represent a conserved tumour suppressive mechanism. - Source: PubMed
Publication date: 2026/08/17
Chaudhari Armi MNguyen Minh ThuNarbonne Patrick - To evaluate time to diagnosis in infants with very early-onset genetic epilepsies, identify contributing factors to diagnostic delay, and assess the impact of a definite diagnosis on clinical management. - Source: PubMed
Publication date: 2026/08/10
Pizzuto ChiaraMorabito ValeriaCarapancea EvelinaCilio Maria Roberta - -related disorders (-RD), caused by variants in encoding the Gαo protein, comprise a broad phenotypic spectrum including movement disorders (MD) and/or epilepsy and are typically associated with developmental delay and intellectual disability. Currently, only symptomatic treatments are available. Zinc can restore guanosine triphosphate hydrolysis and cellular interactions of dysfunctional Gαo. ZINCGNAO1 evaluated the safety and feasibility of oral zinc supplementation in -RD. - Source: PubMed
Publication date: 2026/07/23
Thiel MoritzMartakis KyriakosDuran IbrahimDafsari Hormos SSchiller PetraWeliwitage JithmiHero BarbaraLarasati YonikaKoval AlexeyKatanaev Vladimir LKoy Anne - GNAO1-related disorder is a severe childhood-onset hyperkinetic movement disorder punctuated by life-threatening dyskinetic crises. Small series suggest benefit from bilateral globus pallidus internus deep brain stimulation (GPi-DBS), but optimal timing, patient selection, long-term outcomes, and genotype-specific response remain unclear. We define the clinical impact of GPi-DBS in the largest cohort assembled to date. - Source: PubMed
Publication date: 2026/07/27
Bernardi KaterinaRong JoshNortham Weston TKamińska MargaretHasegawa HarutomoDomínguez-Carral JanaVogt Lindsey MDijk Joke MBeudel MartijnChauvet-Piat ElineSeng Emilie ChanPoulen GaetanMahant NeilGarone GiacomoPauni MicaelaRodríguez JosefinaMunoz-Chesta DanielaJones Hannah FDe la Casa-Fages BeatrizMiranda-Herrero María ConcepciónJennions ElizabethLim Wei KangZea Vera AlonsoMohammad ShekeebSchuurman Rickvan de Pol Laura ARoubertie AgatheIbrahim George MGorodetsky CarolinaThiel MoritzKoy AnneOrtigoza-Escobar Juan DaríoLin Jean-PierreLumsden Daniel EEbrahimi-Fakhari DariusYang Kathryn - The heterotrimeric G proteins are ubiquitous membrane-bound complexes specialized in the transduction of receptor-mediated extracellular signals into intracellular responses. Mutations in the G protein subunit alpha O1 (Gαo), encoded by GNAO1, have been associated with neurodevelopmental disorders characterized by prominent movement disorder with or without epilepsy. The Gnao1[C215Y]/+ mouse model recapitulates key features of the human disease, with a relatively mild phenotype, normal viability and late onset movement abnormalities, detectable in specific motor tasks. Here we report functional alterations in cortical layer V pyramidal neurons from Gnao1[C215Y]/+ mice, with reduction of the inward currents (Ih) and impairment of the GABAB-mediated outward current. We propose an adeno-associated virus (AAV)-based gene therapy aimed at overexpressing the wild-type form of Gαo by intracerebroventricular injection in newborn heterozygous Gnao1[C215Y]/ + mice. Our results demonstrate that overexpression of the wild-type protein mitigates behavioral abnormalities and restores functional neuronal deficits in young adult mice, thereby supporting the development of AAV-mediated gene augmentation strategies to counteract the effects of GNAO1 variants in patients. The potential of gene supplementation therapy is further supported by data from genetically modified C. elegans strains carrying not only the relatively mild C215Y variant but also a panel of goa-1/GNAO1 mutations associated with more severe phenotypes, suggesting a broader potential of this therapeutic strategy. - Source: PubMed
Publication date: 2026/07/21
Cocozza GermanaD'Andrea TizianoDi Rocco MartinaBusdraghi Ludovica MariaChilà GildaLin XingziLanza EnricoCollaud FannyFollo Francesca CBuccheri CleliaFolli ViolaRonzitti GiuseppeScavizzi FerdinandoRaspa MarcelloLeuzzi VincenzoKatanaev Vladimir LGalosi SerenaFucile SergioMartinelli SimoneD'Alessandro GiuseppinaLimatola Cristina