Gria3 antibody - N-terminal region (ARP35200_P050)
- Known as:
- Gria3 (anti-) - N-terminal region (ARP35200_P050)
- Catalog number:
- arp35200_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Gria3 antibody - N-terminal region (ARP35200_P050)
Related genes to: Gria3 antibody - N-terminal region (ARP35200_P050)
- Gene:
- GRIA3 NIH gene
- Name:
- glutamate ionotropic receptor AMPA type subunit 3
- Previous symbol:
- GLUR3
- Synonyms:
- GluA3, GLURC, MRX94
- Chromosome:
- Xq25
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-26
- Date modifiied:
- 2016-02-05
Related products to: Gria3 antibody - N-terminal region (ARP35200_P050)
Related articles to: Gria3 antibody - N-terminal region (ARP35200_P050)
- Cadmium (Cd) is a well-recognized neurotoxic metal whose effects on the central nervous system accumulate with both exposure intensity and duration. However, how dose and time jointly sculpt brain proteome trajectories-and which early molecular events emerge under low-dose, short-duration exposure-remain insufficiently resolved. Time-resolved proteomics can map these trajectories, but requires explicit dose-time deconvolution to separate main effects from interaction-driven changes while accounting for biological heterogeneity. - Source: PubMed
Publication date: 2026/05/02
Hu ZhijianHan FengGao HaoWan ShengLiu HuiJie LiYin YinghuiTian MaoqinYang YongChen WenjieTan XiaoShi XinxinChen QiwenHuang Shaoxin - - Source: PubMed
Publication date: 2026/04/23
Yang FumingWei Jiwu - Understanding how chromosome 21 gene dosage contributes to neurodevelopmental phenotypes in trisomy 21 (T21) remains a fundamental challenge. Here, we perform transcriptome-wide RNA-sequencing of fetal cortical and hippocampal tissues from T21 cases and euploid controls collected during mid-gestation, a critical window for human brain development. We identify widespread gene expression dysregulation with significant enrichment for chromosome 21 genes and perturbation of neurodevelopmental, synaptic, and immune-related pathways. Among the most strongly dysregulated genes is ADARB1, a chromosome 21-encoded RNA editing enzyme, whose overexpression associates with increased adenosine-to-inosine RNA editing, with consistent over-editing at functionally important recoding sites in glutamate and GABA receptor-related genes, including GRIK2, GRIA2, GRIA3, and GABRA3, across cortex and hippocampus. Meta-analyses across independent transcriptomic datasets validate robust chromosome 21 dosage effects, including ADARB1 overexpression and over-editing at 3'UTRs and GRIA3. These findings implicate dysregulated RNA editing as a post-transcriptional mechanism contributing to fetal neuropathology in T21. - Source: PubMed
Publication date: 2026/03/31
Breen Michael SYang AndyWang XuranRodriguez de Los Santos MiguelTao RanWeinberger Daniel RKleinman Joel EMihova KalinaStancheva GerganaSavova SylviaKaneva RadkaDimitrova VioletaVladimirov VladimirHyde Thomas MBuxbaum Joseph D - The expression of the ionotropic glutamate receptors AMPAR and NMDAR has been measured on circulating leucocytes, particularly CD4 lymphocytes, in many studies over the last two decades. As there are agonists and antagonists for these receptors that do not cross the blood brain barrier, they represent potential new avenues to target leucocytes in human disease. To determine the range of expression across pathological conditions, we compared the expression of AMPAR and NMDAR, as well as kainate receptors and metabotropic receptors, in 12 clinical studies including inflammatory autoimmune disease (rheumatoid arthritis, juvenile idiopathic arthritis, lupus and multiple sclerosis), breast cancer, viral infection, schizophrenia and in vitro studies. We measured the expression of AMPAR and NMDAR in freshly isolated CD4 T cells, stimulated PBMC and myeloid cells (HL-60, THP-1 and monocyte-derived macrophages) using TaqMan qPCR. We found the gene expression of glutamate receptors to be negligible with few exceptions. We measured low but reproducible expression of in THP-1 pro-monocytic cells and human blood dendritic cell subsets (pDC, cDC1, cDC2). We observed that AMPA pre-treatment caused a greater inflammatory response in TNF-stimulated THP-1 cells. While these data illustrate a contradiction in the literature, the limited but reproducible expression of glutamate receptors in select immune subsets potentiates peripheral therapeutic targeting in specific disease contexts. - Source: PubMed
Publication date: 2026/03/19
Clanchy Felix I LWilliams Richard OStone Trevor W - BRD1 is an epigenetic regulator implicated in neurodevelopmental and psychiatric disorders, yet its role in human neuronal differentiation, maturation, and function remains poorly understood. Here we show that haploinsufficiency disrupts early neuronal programming, resulting in accelerated maturation and altered neurodevelopmental trajectories in human induced glutamatergic neurons. Transcriptomic profiling reveals an early shift toward neuronal identity, characterized by downregulation of pluripotency markers and persistent upregulation of genes involved in synapse assembly and organization, including . Despite this, neurons form significantly smaller synapses and display increased neuronal activity. Our findings highlight BRD1 as a key regulator of neurodevelopmental timing and synaptic maturation, and network activity reinforcing growing evidence that disruptions in chromatin-mediated control of differentiation and synaptic organization contribute to neurodevelopmental disorders. - Source: PubMed
Publication date: 2026/02/16
Qvist PerDonskov JulieDeans P JPediotidis-Maniatis DimitriosHøgfeldt JacobBorglum AndersDenham MarkBrennand Kristen