GRIN2A antibody - center region (OAAB07577)
- Known as:
- GRIN2A (anti-) - central region (OAAB07577)
- Catalog number:
- oaab07577
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GRIN2A antibody - center region (OAAB07577)
Related genes to: GRIN2A antibody - center region (OAAB07577)
- Gene:
- GRIN2A NIH gene
- Name:
- glutamate ionotropic receptor NMDA type subunit 2A
- Previous symbol:
- NMDAR2A
- Synonyms:
- GluN2A
- Chromosome:
- 16p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-18
- Date modifiied:
- 2016-02-05
Related products to: GRIN2A antibody - center region (OAAB07577)
Related articles to: GRIN2A antibody - center region (OAAB07577)
- Gastric cancer remains a major cause of cancer-related mortality worldwide, highlighting the need for an improved understanding of its molecular mechanisms. Purinergic and glutamatergic signaling pathways, immune checkpoint molecules, and oxidative stress are thought to contribute to tumor biology; however, their combined evaluation in gastric cancer is limited. - Source: PubMed
Publication date: 2026/07/09
Coskun HakkiTuncbilek ZuhalGenc Husnu CagriKaya Gulcihan CinarTas Ayca - Febrile seizures (FS), the most common early-childhood neurological emergency, have a poorly understood impact on the maturing glutamatergic system. We present a detailed spatiotemporal analysis of transcriptional dynamics of key glutamatergic components during a critical postnatal window. Using a hyperthermia-induced FS model in rats at postnatal day 10, we measured mRNA levels of ionotropic (NMDA, AMPA) subunits, metabotropic glutamate receptor (mGluR) groups I-III, glutamate transporters (Slc1a1-3), and glutamine synthetase (Glul) across the dorsal/ventral hippocampus, temporal and medial prefrontal cortices at P14, P21, and P50. For selected targets (GluN2A/2B, GluA1/2, EAAT2), protein abundance was analyzed by Western blotting to test how closely transcriptional changes are reflected at the protein level. We identified robust region- and age-specific developmental trajectories for all targets, including the expected maturational shift in NMDA receptor subunits. FS disrupted these programs, causing widespread downregulation of NMDA and AMPA receptor subunits, mGluRs, and astrocytic transporters in the dorsal hippocampus and temporal cortex at P14. Importantly, FS prevented the normal developmental increase in the Grin2a/Grin2b mRNA ratio in the dorsal hippocampus at P21. Notably, protein abundance for selected targets did not mirror transcriptional changes at the examined time points, suggesting post-transcriptional buffering or delayed translation. This mismatch suggests that transcriptional changes may precede detectable proteomic alterations during circuit maturation, although alternative explanations, such as delayed translation or post-translational regulation, cannot be excluded. Our findings identify candidate transcriptional correlates that may contribute to long-term neurocognitive vulnerability, and highlight the potential importance of timing when targeting glutamatergic pathways for neuroprotection. - Source: PubMed
Publication date: 2026/07/25
Kovalenko Anna AZakharova Maria VSchwarz Alexander PZubareva Olga EZaitsev Aleksey V - Cognitive flexibility-the ability to adapt behavior when contingencies change-is impaired in psychiatric disorders involving prefrontal dysfunction. The medial prefrontal cortex (mPFC) relies on noradrenergic input from the locus ceruleus (LC), yet the molecular mechanisms enabling this neuromodulatory control remain unclear. Here we show that GluN2A-containing NMDA receptors are required for LC-mPFC regulation of network dynamics and reversal learning in male mice. Optogenetic activation of LC→mPFC projections enhanced reversal learning in wild-type (WT) and heterozygous mice but not in global knock-outs, whereas LC inhibition impaired performance only in WT animals. In slices, norepinephrine (NE) and LC stimulation induced gamma and high-frequency oscillations in WT mPFC that were blocked by α2-adrenergic antagonism, but these oscillatory responses were undetectable in mutants. mutants also exhibited increased LC axonal density and elevated NE transporter expression in the prelimbic cortex, consistent with enhanced noradrenergic clearance capacity. Together, these findings identify GluN2A as a key determinant of LC-prefrontal circuit function supporting cognitive flexibility. They suggest that functional deficits in these mutants should be interpreted within the context of compensatory structural hyperinnervation resulting from global GluN2A deficiency, which may reflect a developmental adaptation rather than acute signaling loss. Furthermore, these results promote α2-adrenergic pathways as potential entry points for restoring prefrontal network coordination. - Source: PubMed
Publication date: 2026/08/07
Hosseini HassanEvans-Martin SkyBogomilsky EmmaJones Kevin S - Opioid use disorder (OUD) remains a critical global health challenge. The nucleus accumbens (NAc), a key region of the brain reward system, plays an essential role in opioid-induced neuroadaptations. Characterizing gene expression alterations in reward-system regions, such as the NAc, is essential for elucidating the molecular mechanisms underlying addiction. In recent years, bioinformatics has emerged as a rapidly advancing field and has played a pivotal role in elucidating molecular mechanisms and in advancing computational biology. - Source: PubMed
Publication date: 2026/06/02
Pourmand Seyed MahmoudNazari ShahrzadNazari ElhamArezoomandan RezaHassanzadeh GholamrezaEshrati SaharKarami-Zarandi MortezaSaberi-Zafarghandi Mohammad Bagher - Atrazine (ATZ) is a triazine herbicide and a persistent environmental contaminant. Its use is associated with effects on the nervous system in experimental models. Behavioral and molecular alterations have been reported after exposure, but the cellular mechanisms underlying atrazine-induced developmental neurotoxicity remain unclear, particularly at the synaptic level. In this study, we investigated the effects of ATZ exposure on glutamatergic synaptic maturation in rat primary hippocampal neurons. Neuronal cultures were exposed to ATZ throughout the in vitro developmental period, and structural and molecular endpoints were assessed. Dendritic spines were analyzed by confocal microscopy, and the expression of glutamatergic receptor subunits was evaluated by Western blot and RT-qPCR. In parallel, microRNA expression profiles targeting NMDA receptor subunits were examined to explore post-transcriptional regulatory mechanisms. ATZ exposure induced a selective reduction in dendritic spine density, without detectable changes in spine morphology. This structural effect was accompanied by a selective decrease in the NMDA receptor subunit GluN2A at both protein and mRNA levels, while GluN1, GluN2B, and AMPA receptor subunits were unaffected. Notably, GluN2A downregulation was preceded by the upregulation of microRNAs predicted to target the GRIN2A transcript, indicating a microRNA-mediated regulatory mechanism. Overall, these results demonstrate that ATZ can interfere with hippocampal synaptic maturation by selectively modulating NMDA receptor subunit composition through epigenetic mechanisms. This study identifies dendritic spine and GluN2A regulation as sensitive endpoints of ATZ-induced developmental neurotoxicity and provides mechanistic insight into how early synaptic processes may be affected by this herbicide. - Source: PubMed
Publication date: 2026/07/14
Serafini Melania MariaGraziosi AgneseMidali MiriamGhelli LucaGrumelli GiacomoSita GiuliaCorsini EmanuelaMarinovich MarinaMorroni FabianaViviani Barbara