GNAO1 antibody
- Known as:
- GNAO1 (anti-)
- Catalog number:
- orb39825
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- GNAO1 antibody
Related genes to: GNAO1 antibody
- 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
Related articles to: GNAO1 antibody
- The gene is located on the long arm of chromosome 16 (16q13) and is associated with Developmental and Epileptic Encephalopathy 17. It encodes a protein involved in regulating various neurotransmitters and neuronal growth and development. The 16p13.11 microdeletion is a genomic deletion in the p13.11 region of the short arm of chromosome 16, previously reported to predispose individuals to neurodevelopmental disorders. These two regions do not overlap on the chromosome, and the 16p13.11 microdeletion does not involve the gene locus. - Source: PubMed
Publication date: 2026/08/28
Liu XuanLuo RongWang JianjunChen XiaoluDeng Yao - Childhood-onset movement disorders comprise a heterogeneous group of rare conditions with substantial unmet therapeutic needs. Recent advances in disease gene discovery, mechanistic modeling, and translational platforms have accelerated the development of targeted therapies and enabled innovative clinical trial designs for small patient populations. To review novel and emerging therapies for childhood-onset movement disorders, with a focus on pharmacologic strategies, disease-modifying approaches, and patient-centered precision therapies. We surveyed the literature, major conference proceedings, and expert networks to identify therapies approved, in clinical development, or supported by compelling preclinical data between 2022 and 2025. We focused on small molecules and genetic therapies for conditions in which movement disorders represent a prominent clinical feature. Small molecules were categorized as repurposed or novel drugs, whereas genetic therapies included gene replacement, gene editing, and RNA-based expression modulation. Drug repurposing approaches have shown promise in disorders related to the GNAO1, ATP1A3, ATM, and ADCY5 genes. Novel small molecules have advanced for Friedreich's ataxia and Tourette's syndrome. Gene replacement therapies have demonstrated clinical benefit in select neurotransmitter disorders, whereas gene editing strategies have entered preclinical development for ATP1A3-related disease. Antisense oligonucleotide therapies have yielded encouraging early results across several conditions with prominent movement disorder phenotypes, including KIF1A-related neurological disorder, Angelman syndrome, SCN2A-related neurodevelopmental disorder, and ataxia-telangiectasia. Precision-based therapeutic strategies are rapidly reshaping the treatment landscape for childhood-onset movement disorders. Continued progress will depend on rigorous phenotyping, careful ethical oversight, and deliberate efforts to promote equitable global access to emerging therapies. © 2026 International Parkinson and Movement Disorder Society. - Source: PubMed
Publication date: 2026/09/11
de Gusmao Claudio MKatanaev Vladimir LSilveira-Moriyama LauraPringsheim TamaraRoze Emmanuel - 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