VIAAT (Vesicular Inhibitory Amino Acid Transporter) Antibody
- Known as:
- VIAAT (Vesicular Inhibitory Amino Acid Transporter) Antibody
- Catalog number:
- 20092
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Immunostar
- Gene target:
- VIAAT (Vesicular Inhibitory Amino Acid Transporter) Antibody
Related genes to: VIAAT (Vesicular Inhibitory Amino Acid Transporter) Antibody
- Gene:
- SLC32A1 NIH gene
- Name:
- solute carrier family 32 member 1
- Previous symbol:
- VIAAT
- Synonyms:
- VGAT, bA122O1.1
- Chromosome:
- 20q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-20
- Date modifiied:
- 2016-10-05
Related products to: VIAAT (Vesicular Inhibitory Amino Acid Transporter) Antibody
Related articles to: VIAAT (Vesicular Inhibitory Amino Acid Transporter) Antibody
- Sleep pressure is regulated not only by circadian rhythms, but also by sleep homeostasis, an activity-dependent process that dissipates during sleep. Recent work implicates -positive GABAergic neurons of the zona incerta (ZI) in regulating sleep pressure, but their precise role remains unclear. Using sleep deprivation and HiPlex single-molecule fISH, we show that -positive ZI neurons are broadly activated by both natural and induced increases in sleep pressure and remain active for more than 3 h into recovery sleep. Anterior -positive neurons showed stronger activation. induction differed across molecularly distinct subpopulations, with -positive cells showing robust responses and -positive cells showing reduced activation. We also identified distinct sleep pressure-responsive Lhx6-negative -positive GABAergic ZI subpopulations. Finally, intersectional genetic loss of reduced and redistributed -positive neurons, blunted their activation, and increased total sleep time. These findings reveal a central, heterogeneous role for -positive ZI neurons in sleep homeostasis. - Source: PubMed
Publication date: 2026/03/19
Chandler Parris WashingtonLee Sang SooDuncan Leighton HKim Dong WonWu MarkBlackshaw Seth - Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by memory and cognitive decline. Recent studies highlight the significant role of microRNAs (miRNAs) in regulating genes related to AD. This research aims to develop miRNA-associated gene regulatory networks as candidate AD biomarkers. - Source: PubMed
Publication date: 2026/03/06
Pan ShujuanZhou YanfangWang XiaoyuTong JinghuiLi YanliHuang JunchaoChen SongCui YiminWang ZhirenTan Yun-Long - - Source: PubMed
Publication date: 2026/03/11
Yu YunWu YaoyueZhao HuairenZhou ZijuanBai JingZhang YuedongZhang FengyunZhou BowenWang JingyuZhang Ya-Ping - Obsessive-compulsive disorder (OCD) is a chronic psychiatric illness associated with altered function in cortico-striatal-thalamo-cortical (CSTC) circuits. In this pilot study, we examined differential RNA expression in the thalamus using postmortem human brain tissue samples from 11 subjects with OCD and 10 unaffected subjects. We individually dissected the mediodorsal magnocellular, mediodorsal parvocellular, and ventral anterior nuclei, which participate in orbitofrontal and anterior cingulate CSTC circuits most frequently associated with OCD, and the posterior ventrolateral nucleus, which participates in premotor and motor circuits that are increasingly implicated in OCD. Preselected GABAergic, glutamatergic and ion channel genes were analyzed via qPCR. Two genes required for GABA synthesis and release, GAD1 and SLC32A1, were found to be downregulated in OCD subjects across all nuclei, and potassium channel KCNN3 was upregulated. In parallel, we performed an exploratory total RNAseq differential expression analysis. We identified few (12-52) differentially expressed genes (DEGs) in each nucleus, and only one DEG in a pooled analysis of all nuclei. No DEGs were significant after correction for multiple comparisons. Investigation by model selection indicated that OCD diagnosis was not a useful factor in modelling gene expression in our dataset. OCD was also not associated with any modules of co-expressed genes identified using weighted gene correlation network analysis. Overall, we found minimal evidence of differential RNA expression in these thalamic nuclei in OCD. These findings contrast with our previous work including many of the same subjects where we found widespread differential mRNA expression in the orbitofrontal cortex and striatum in OCD. - Source: PubMed
Publication date: 2026/02/06
Springer Shale ADeshmukh RishiKlei LambertusDevlin BernieGlausier Jill RLewis David AAhmari Susanne E - This study explores the cell fate reprogrammability of H3K27M-mutant pediatric high-grade gliomas (pHGG) using neuronal transdifferentiation as a potential targeted therapy. We treated the BT245 patient-derived glioma cell line with pharmacological combinations targeting neuronal differentiation pathways and performed bulk RNA sequencing to characterize gene expression patterns driving cell fate transitions. Our findings reveal that the drug combinations induce transcriptomic changes consistent with differentiation towards neuronal phenotypes, including the upregulation of synaptic and dendritic signaling genes and the downregulation of malignant signatures. In comparison, astrocytic differentiation media (DM) and H3K27M knockout (KO) promote residual astrocytic phenotypes, suggesting neuronal transdifferentiation as a more effective strategy for mitigating tumor aggressiveness and progression. Differentially expressed genes such as GRIK1, GRIN1, NRXN3, NRXN1, CALB2, SCGN, SLC32A1, SLC1A2, KCNC3, and neurodevelopmental regulators including WNT7A, DLX6, ERBB4, ARX, BCL11B, SEMA3C, and FGFBP3 were identified as key markers regulating the neuron-like lineage transition. This study demonstrates that pHGGs can be phenotypically redirected toward neuronal-like identities through modulating cell fate differentiation programs. These findings advance the concept of 'differentiation therapy' as a promising intervention to reduce phenotypic plasticity and malignancy in pHGG ecosystems. While these are early in vitro findings, the potential ability to steer and control glioma cells toward stable, less malignant fates offers promising translational potential for patient-centered targeted therapies. - Source: PubMed
Publication date: 2025/12/30
Uthamacumaran AbicumaranHorth CynthiaBareke EricGravel MichelMajewski Jacek