Ask about this productRelated genes to: VMAT2 antibody
- 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: VMAT2 antibody
Related articles to: VMAT2 antibody
- 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 - Brain monoamine vesicular transporter deficiency is a rare autosomal recessive neurometabolic disorder caused by mutations in the gene, which encodes vesicular monoamine transporter 2 (VMAT2). VMAT2 is essential for packaging neurotransmitters such as dopamine, serotonin, norepinephrine, and histamine into synaptic vesicles. Its deficiency results in disrupted neurotransmission and a characteristic clinical syndrome involving developmental delay, hypotonia, movement disorders, and autonomic dysfunction. We report a novel homozygous frameshift variant, Chr10:119014792dupC (p.Phe238LeufsTer7), identified in a 5-month-old male from a consanguineous family, who presented with severe hypotonia, oculogyric crises, and developmental delay. This variant expands the known genotypic spectrum of -related disease. Our findings underscore the importance of early genetic testing in infants with unexplained movement disorders and support a multidisciplinary approach to care. We also compare this case to related neurometabolic disorders with overlapping clinical features and with prior mutation-related disorder. - Source: PubMed
Publication date: 2026/03/10
Brewer SophiaRamani Praveen KumarArya Kapil - 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 0.14-0.38 across eleven 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 , , and (chromosome 1); and (chromosome 14); and and (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
Publication date: 2026/02/19
Chitre Apurva SHebda-Bauer Elaine KEmery Michael ALi FeiNguyen Khai-MinhWang YizhiCheng RiyanPolesskaya OksanaWatson Stanley JLi JunAkil HudaPalmer Abraham A - Parkinson's disease (PD) is characterized by α-synuclein accumulation and dopaminergic neuron degeneration, with dopamine (DA) oxidation emerging as a key pathological driver. However, the mechanisms underlying this neurotoxic process remain unclear. Using PD patient-derived and CRISPR-engineered induced pluripotent stem cell midbrain dopaminergic neurons lacking DJ-1, we identified defective sequestration of cytosolic DA into synaptic vesicles, which culminated in DA oxidation and α-synuclein pathology. In-depth proteomics, state-of-the-art imaging, and ultrasensitive DA probes uncovered that decreased vesicular monoamine transporter 2 (VMAT2) protein and function impaired vesicular DA uptake, resulting in reduced vesicle availability and abnormal vesicle morphology. Furthermore, VMAT2 activity and vesicle endocytosis are processes dependent on adenosine 5'-triphosphate (ATP), which is notably reduced in DJ-1-deficient dopaminergic neurons. ATP supplementation restored vesicular function and alleviated DA-related pathologies in mutant dopaminergic neurons. This study reveals an ATP-sensitive mechanism that regulates DA homeostasis through VMAT2 and vesicle dynamics in midbrain dopaminergic neurons, highlighting enhanced DA sequestration as a promising therapeutic strategy for PD. - Source: PubMed
Publication date: 2026/02/11
Heger Leonie MGubinelli FrancescoHuber Andreas JCardona-Alberich AidaRovere MatteoMatti UlfMüller Stephan ANagaraja Sankarshana RJaschkowitz LenaSchifferer MartinaWurst WolfgangLichtenthaler Stefan FBehrends ChristianSambandan SivakumarBurbulla Lena F