SLC18A2 _ VMAT2
- Known as:
- SLC18A2 _ VMAT2
- Catalog number:
- VMAT21-A
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SLC18A2 _ VMAT2
Related genes to: SLC18A2 _ VMAT2
- Gene:
- SLC18A2 NIH gene
- Name:
- solute carrier family 18 member A2
- Previous symbol:
- VMAT2
- Synonyms:
- SVMT, SVAT
- Chromosome:
- 10q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-25
- Date modifiied:
- 2016-10-05
Related products to: SLC18A2 _ VMAT2
Anti- Vesicular Monoamine Transporter (VMAT2) AntibodyAnti- Vesicular Monoamine Transporter (VMAT2) AntibodyAnti-Rat Vesicular Monoamine Transporter 2 (VMAT2) ab #1, aff pureAnti-Rat Vesicular Monoamine Transporter 2 (VMAT2) antiserum #2anti-SLC18A2anti-SLC18A2anti-SLC18A2 type: Primary antibodies host: MouseAnti-VMAT2 AntibodyAnti-VMAT2 antibodyAntibodies: VMAT2 _ SLC18A2 HOST: Goat Clonality: pAbAnti_Rat Vesicular Monoamine Transporter 2 (VMAT2) ab 1, aff pureAnti_Rat Vesicular Monoamine Transporter 2 (VMAT2) antiserum 2Bos taurus,Bovine,Monoamine transporter,SLC18A2,Solute carrier family 18 member 2,Synaptic vesicular amine transporter,VAT2,Vesicular amine transporter 2,VMAT2Bovine solute carrier family 18 (vesicular monoamine), member 2 (SLC18A2) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine Synaptic vesicular amine transporter(SLC18A2) ELISA kit Related articles to: SLC18A2 _ VMAT2
- Parkinsons disease, characterized by the aggregation of alpha-synuclein is a complex neurodegenerative disorder with the fastest global prevalence growth. The identification of shared genes expressed in both blood and brain of Parkinson's disease patients improves the knowledge on peripheral pathophysiology of the disease and facilitates identification of minimally invasive potential biomarkers from these shared genes. Our study intends to identify a shared transcriptomic signature between the blood and brain critical for developing minimally invasive biomarkers and understanding systemic disease progression. This study implemented an integrative bioinformatic approach towards the public microarray dataset comprising of both human Parkinson's disease blood and post-mortem brain cohorts. After routine data preparation and differential gene expression analysis across tissues, functional annotation, protein-protein interaction networks, and topological hub analysis were utilized to delineate underlying systemic pathways. A robust nine-gene signature-ANK1, CMAS, GUCY1B1, PRKAR2B, PSD3, RAB27B, SLC18A2, SNCA, and UCHL1-was downregulated in both blood and brain tissue, as demonstrated by the comparative gene expression analysis. Functional enrichment revealed a fundamental impairment in vesicle processing and synaptic maintenance, implying a failure in the cellular mechanisms necessary for neurotransmitter transport and the removal of protein aggregates-both of which play a crucial role in the neurodegenerative advancement of Parkinson's Disease. Non-compensated cellular homeostatic collapse indicated by concurrent decreases in RAB27B (vesicular clearance), UCHL1 (protein recycling), and SLC18A2 (synaptic transmission). NANOG, SNCA, UCHL1, SLC18A2, and ANK1 were found to be important regulatory hubs by topological analysis. This coordinated downregulation offers molecular evidence of an uncompensated systemic homeostatic failure in Parkinson's disease. - Source: PubMed
Publication date: 2026/10/02
Mohammad HafsaSingh AkankshaBansal Dipika - N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD) and its oxidation product 6PPD-Q are emerging tire-derived environmental contaminants that have been detected in human biological samples; however, their neurotoxic mechanisms remain unclear. This study employed network toxicology, transcriptomic analysis, and machine learning to explore the potential neurotoxic associations between 6PPD/6PPD-Q and Parkinson's disease (PD). By integrating four target prediction platforms and three disease databases, a total of 260 potential toxic targets associated with 6PPD/6PPD-Q-related PD were identified. Eighty-two differentially expressed genes were identified from GEO datasets, and five candidate genes were obtained through intersection analysis. Among the five candidate genes, KCND3, PSEN2, and SLC18A2 were consistently selected by three machine-learning algorithms (LASSO, SVM-RFE, and Boruta). Validation analysis showed that all core genes were significantly downregulated in the substantia nigra tissues of PD patients, with area under the curve (AUC) values of 0.917 for KCND3, 0.757 for PSEN2, and 0.819 for SLC18A2. Mendelian randomization analysis provided preliminary genetic evidence consistent with a causal association between elevated SLC18A2 expression levels and reduced PD risk (OR = 0.488, 95% CI: 0.273-0.870, P = 0.015). Molecular docking analysis showed favorable predicted binding scores between 6PPD/6PPD-Q and the three target proteins. Exploratory immune analysis suggested alterations in activated dendritic cells and γδ T cells in PD. Collectively, these findings suggest potential neurotoxic relevance of 6PPD/6PPD-Q to PD and provide a basis for further experimental investigation. - Source: PubMed
Publication date: 2026/10/01
Zhang LijuanPeng BowenHua DaipingXuan QiaoyuSun LantingYang WenmingWang Han - Neurodegenerative diseases, particularly Alzheimer's disease, Parkinson's disease and Huntington's disease are characterized by progressive neuronal loss driven by complex mechanisms such as oxidative stress, neuroinflammation, protein aggregation, neurotransmitter imbalance, and synaptic dysfunction. Among these, Alzheimer's disease remains the most prevalent and challenging disorder, lacking effective disease-modifying therapies. Quercetin, a naturally occurring flavonoid abundant in fruits and vegetables, has attracted considerable attention due to its potent antioxidant, anti-inflammatory, anti-apoptotic, and neuroprotective properties, along with its ability to cross the blood-brain barrier. This review critically examines the potential role of quercetin in modulating key pathological pathways in neurological disease, with a special focus on its interaction with the vesicular monoamine transporter 2 (VMAT2). Vesicular monoamine transporter 2 plays a crucial role in maintaining monoamine neurotransmitter homeostasis and protecting neurons from oxidative damage caused by cytosolic monoamine degradation. Increasing data indicates that VMAT2-mediated dysfunction represents one of multiple processes that lead to neurotoxicity by altering monoamine synthesis, increasing oxidative damage, and leading to synaptic damage, especially in neuronal pathways. Quercetin, as a potential monoamine oxidase inhibitor and reactive oxygen species scavenger, may indirectly preserve vesicular monoamine transporter 2 function and mitigate downstream neurotoxic events. Overall, the multitargeted actions of quercetin, combined with its potential influence on vesicular monoamine transporter 2-mediated pathways, highlight its promise as a complementary therapeutic candidate for further neurodegenerative disorders. An increasing number of studies demonstrates that quercetin may indirectly regulate VMAT2 function by eliminating reactive oxygen compounds, decreasing neuroinflammation, inhibiting monoamine oxidase activity, improving mitochondrial activity, and maintaining monoaminergic neuronal function, although there remains limited direct evidence connecting quercetin to VMAT2 regulation. The substance quercetin can reduce oxidative neuronal damage and decrease subsequent neurodegenerative events through several connected methods. Although direct experimental verification of the quercetin-VMAT2 connection is still lacking, the data that is now accessible suggests that VMAT2 may be a suitable target for further research. Therefore, the suggested quercetin-VMAT2 connection should be seen as a hypothetical and mechanistic approach. - Source: PubMed
Publication date: 2026/08/28
Sharma KanishkaVikram VirJamwal PallaviBhaumik SoumyadeepPrasad NitinRohit Juneja Rinka - Parkinsonism-dystonia Type 2 (PKDYS2) is a rare autosomal recessive disorder caused by variants affecting the vesicular monoamine transporter 2 (VMAT2). We report the first genetically confirmed Iranian patient, an 18-month-old boy presenting with profound developmental delay, axial hypotonia, limb hypertonia, dystonia, oculogyric crises, ptosis, and autonomic dysfunction. Brain MRI, metabolic studies, and neurophysiological evaluations were normal. Whole-exome sequencing identified a novel homozygous canonical splice-site variant in (NM_003054.6:c.1071-2A > G), confirmed by Sanger sequencing and absent from population databases. SpliceAI predicted loss of the native splice acceptor site (DS_AL = 0.74), supporting a deleterious effect on RNA splicing. According to ACMG criteria, the variant was classified as likely pathogenic. Levodopa-benserazide failed to provide sustained benefit and caused irritability and insomnia, whereas pramipexole produced modest improvement in bradykinesia, ptosis, and sweating with persistence of dystonia and oculogyric crises. Comparison with reported international cases shows a consistent phenotype and limited therapeutic response. This case expands the mutational spectrum of -related disease and highlights the importance of early genetic diagnosis. - Source: PubMed
Publication date: 2026/08/25
Nikkhah AliBadv Reza ShervinHabibi Seyed Amir HasanZorzi GiovannaMehdizadeh Maryam - Vesicular monoamine transporter 2 (VMAT2) transports monoamines into storage vesicles. We have previously reported that VMAT2 negatively regulates pancreatic progenitor differentiation into endocrine beta cells; however, the underlying mechanism remains unknown. Using a pancreatic bud explant culture, we show here that inhibiting VMAT2-mediated catecholamine uptake promotes pancreatic epithelial branching and increases the number of insulin-expressing cells. The increase in pancreatic branching was mimicked by inhibition of tyrosine hydroxylase, monoamine oxidase A, dopamine beta-hydroxylase or norepinephrine transporter. RNA sequencing analysis of the pancreatic buds revealed that reactive oxygen species (ROS) play a role in branch formation. We found that these early glucagon (GCG) and insulin (INS) co-expressing cells express VMAT2 and monoamine signaling components. Lineage-specific VMAT2 deletion in Gcg-expressing cells resulted in increased pancreatic branching and islet areas, and decreased ROS accumulation. We conclude that early GCG and INS co-expressing cells regulate pancreatic branching morphogenesis via VMAT2-noradrenaline-mediated ROS signaling. - Source: PubMed
Publication date: 2026/09/11
Inoue AiriUefune FumiyaShitamichi TakahiroSakano DaisukeKume Shoen