Ask about this productRelated genes to: GRIA2 Blocking Peptide
- Gene:
- GRIA2 NIH gene
- Name:
- glutamate ionotropic receptor AMPA type subunit 2
- Previous symbol:
- GLUR2
- Synonyms:
- GluA2, GLURB
- Chromosome:
- 4q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-26
- Date modifiied:
- 2016-02-05
Related products to: GRIA2 Blocking Peptide
Related articles to: GRIA2 Blocking Peptide
- Histone deacetylases (HDACs) regulate neuroprotection; however, Trichostatin A (TSA), an HDAC inhibitor, lacks clear molecular mechanisms and core targets in Alzheimer's disease (AD), limiting clinical translation. This study aimed to decipher TSA's AD-regulating network, screen core genes, and support AD early diagnosis and multi-target therapies. - Source: PubMed
Publication date: 2026/04/20
Ou ChangzeChen BinbinDeng JunLong Huajun - 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 - Epithelial-myoepithelial carcinoma (EMC) is a rare malignant tumor of the salivary glands, often characterized by HRAS mutations. The present study aimed to better define the molecular and transcriptomic landscape of EMC and explore its relationship with other head and neck neoplasms, particularly basal cell adenoma (BCA). We retrospectively analyzed 14 EMC cases using histology, immunohistochemistry, and whole-exome capture RNA sequencing. HRAS mutations were identified in 57.0% (8/14) of EMC, predominantly at p.Gly61Arg. Additional mutations identified included PIK3CA, STAT5B, and NOTCH1, as well as gene fusions such as HMGA2::WIF1 and FBXO32::PLAG1. A comparative analysis with 54 RAS-mutated head and neck tumors revealed that HRAS mutations were not exclusive to EMC, as they were also found in benign entities such as BCAs. Transcriptomic profiling found that EMC and BCA shared significant gene expression similarities, clustering closely. Differential expression analysis found upregulation of GATA3, CHI3L1, GRIA2, and MME in EMC, while BCAs had enrichment of Wnt-beta-catenin signaling. In contrast, EMCs had activation of the Ras-Raf-MAPK and PI3K-Akt pathways, supported by upregulation of E2F and G2-M checkpoint targets. Immunohistochemistry confirmed GATA3 positivity in HRAS-mutated EMCs. The frequent RAS mutations and overlapping transcriptomic profiles raise important diagnostic considerations and highlight the need for integrated molecular analyses to differentiate these entities. The EMCs displayed a recurrent HRAS mutation, also observed in other head and neck tumors, and were partially clustered with the cases of BCA, suggesting potential biological similarities. - Source: PubMed
Publication date: 2026/03/25
Alsugair ZiyadDescotes FrançoiseChampagnac AnneLopez JonathanFieux MaximePhilouse PierreCéruse PhilippeThamphya BricePissaloux DanielTirode FranckBenzerdjeb Nazim - - Source: PubMed
Publication date: 2026/03/24
Biradar Prakash RNaik SnehaDwivedi Prarambh S RMallur Rajat SMole Shruti SHungund Bhagyashri - Chronic fluorosis can cause injury to the central nervous system. Because fat mass and obesity-associated protein (FTO) connected with demethylation of N6-methyladenosine (m6A) plays a crucial role in maintaining brain function, we examined whether FTO might help resist the neurotoxicity of fluoride. Sprague-Dawley rats with chronic fluorosis and cultured nerve cells exposed to fluoride with overexpression or knockdown of FTO were employed. The Morris water maze test was employed to assess learning and memory. Expressions of FTO, m6A, postsynaptic density protein 95 (PSD95) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPARs) and its subunit GluR2 mRNA stability, apoptosis, and reactive oxygen species (ROS) were determined by Western blotting, RT-PCR, and biochemical methods, respectively. The results showed that the impaired learning and memory of rats with chronic fluorosis, the decreased FTO, PSD95 and AMPARs, the elevated m6A, and the disrupted synapse morphology as well as apoptosis in their brains were determined. Similar abnormal changes were further confirmed in primary neurons and SH-SY5Y cells exposed to fluoride, accompanied by a significant decline of GluR2 and high ROS. Notably, overexpression of FTO reduced m6A, enhanced GluR2, and attenuated neurotoxicity induced by fluoride, whereas knockdown had the opposite effects. FTO can alleviate the neurotoxicity induced by fluoride, in which the mechanism may be involved in its regulating m6A to enhance expression of GluR2. - Source: PubMed
Zeng Xiao-XiaoHe Wen-WenLiao WeiXiao XiaoTu XiDeng JieQi Xiao-LanDong Yang-TingHong WeiHe YanXiao YanWei NaGuan Zhi-Zhong