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
- Monoamine neurotransmitter disorders are rare, early-onset neurological conditions that frequently mimic cerebral palsy or epileptic encephalopathies, resulting in diagnostic delay. Parkinsonism-dystonia-2 (PKDYS2), caused by biallelic variants in , encodes vesicular monoamine transporter 2 (VMAT2), which is essential for dopamine and serotonin vesicular storage and release. The disorder is characterized by global developmental delay, parkinsonism, dystonia, and autonomic dysfunction. - Source: PubMed
Publication date: 2026/05/21
Almutair MeshalHakami Wejdan - Parkinson's disease (PD) involves progressive dopaminergic neuron loss in the substantia nigra (SN). Aldehyde dehydrogenase 1A1 (ALDH1A1), the rate-limiting enzyme in retinoic acid biosynthesis, is enriched in vulnerable dopaminergic neuron subpopulations and is consistently downregulated in PD. However, the relationship between ALDH1A1 expression and broader dopaminergic pathway gene co-expression has not been systematically characterized across multiple independent datasets. - Source: PubMed
Publication date: 2026/05/19
Harbert Drake H - Studies have shown that substance use liability is associated with novelty seeking, anxiety-like behavior, and pain sensitivity. We examined whether common genetic variation in outbred Sprague-Dawley rats explained variation in behavioral measures from three assays with established links to substance use: locomotor response to a novel environment, elevated plus maze, and tail flick. We estimated single-nucleotide polymorphism heritability and performed genome-wide association analyses using permutation-derived significance thresholds (N = 534-654 rats across traits). Heritability estimates ranged from 0.14 to 0.38 across 11 traits. Three independent loci were identified: chromosome 1 for elevated plus maze open-arm behavior (α = 0.05), chromosome 14 for elevated plus maze immobility (α = 0.10), and chromosome 17 for tail flick latency (α = 0.05). Candidate genes included Slc18a2, Gfra1, and Pdzd8 (chromosome 1); Rel and Bcl11a (chromosome 14); and Eci2 and Eci3 (chromosome 17). We compared these loci with our genome-wide association study of a F intercross of selectively bred high- and low-responder rats, originally derived from Sprague-Dawleys, that model individual differences in externalizing and internalizing behavior. The current loci are distinct from the ones identified in the bred lines. This difference likely reflects selection history in the high- and low-responder Fs, which focused on facets of exploratory locomotion, while loci for anxiety and pain sensitivity traits were identified in the outbreds. This highlights the benefit of using both outbred and selectively bred rats to probe causal variants contributing to individual differences in substance use liability. The current outbred findings implicate monoaminergic signaling, transcriptional control, and lipid metabolism as testable mechanisms for addiction-relevant behaviors. - Source: PubMed
Chitre Apurva SHebda-Bauer Elaine KEmery Michael ALi FeiNguyen Khai-MinhWang YizhiCheng RiyanPolesskaya OksanaWatson Stanley JLi JunAkil HudaPalmer Abraham A - Lidocaine, a widely used local anesthetic, has been reported to exert anti-cancer activity against hepatocellular carcinoma (HCC). However, its molecular mechanisms remain incompletely understood. This study sought to elucidate the mechanisms underlying lidocaine’s effects on HCC. Potential lidocaine targets in HepG2 cells were identified using network pharmacology and transcriptomic profiling. The prognostic and clinical relevance of candidate genes were assessed through bioinformatics analyses. Key targets were validated by RT–qPCR. The functional role of SLC6A3 in regulating HepG2 cell proliferation, apoptosis, migration, and invasion was examined through in vitro assays. Network pharmacology predicted 433 lidocaine targets, while transcriptomic profiling revealed 442 differentially expressed genes. Nine overlapping targets (SLC6A3, CHRNB2, GRIN1, ADRA2C, LIPE, SLC18A2, KCNQ2, TERT, and ALOX12) were enriched in pathways associated with neuronal signaling, synaptic transmission, and drug addiction. Among these, SLC6A3 and TERT were significantly associated with poor prognosis and increased tumor immune infiltration. Both genes demonstrated predictive value for 1- to 2-year survival, with SLC6A3 showing the stronger prognostic relevance. Molecular docking revealed hydrophobic interactions between lidocaine and SLC6A3 (binding energy: −5.6 kcal/mol). Silencing of SLC6A3 markedly promoted apoptosis and suppressed proliferation, migration, and invasion of HepG2 cells. Collectively, these findings suggest that lidocaine inhibits HCC progression by targeting and downregulating SLC6A3. Lidocaine exerts anti-HCC effects by directly targeting and downregulating SLC6A3, thereby inducing apoptosis and suppressing tumor progression. - Source: PubMed
Publication date: 2026/04/07
Li PeiyangTong WulanHe HongLiu HaoYang Xi - - Source: PubMed
Publication date: 2026/04/06
Yoganathan SangeethaAlFaris Haya SVogt LindseyEid MicheleMenetrey AnikaChowdhury Sayoni RoyCodeiro DawnKrishnan PradeepAljouda LialiTam Emily W YGorodetsky Carolina