SLC1A2 antibody - middle region (ARP33841_P050)
- Known as:
- SLC1A2 (anti-) - middle region (ARP33841_P050)
- Catalog number:
- arp33841_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SLC1A2 antibody - middle region (ARP33841_P050)
Related genes to: SLC1A2 antibody - middle region (ARP33841_P050)
- Gene:
- SLC1A2 NIH gene
- Name:
- solute carrier family 1 member 2
- Previous symbol:
- -
- Synonyms:
- GLT-1, EAAT2
- Chromosome:
- 11p13
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-15
- Date modifiied:
- 2016-02-17
Related products to: SLC1A2 antibody - middle region (ARP33841_P050)
Related articles to: SLC1A2 antibody - middle region (ARP33841_P050)
- Neuropathic pain is associated with anxiety-like disorders, suggesting shared neurobiological mechanisms. Glutamatergic dysregulation and impaired astrocytic glutamate uptake, particularly via the astrocytic transporter GLT-1, have been implicated in central sensitization and associated affective disorders. Ceftriaxone, a β-lactam antibiotic known to enhance GLT-1 expression, may represent a potential strategy to alleviate pain-related anxiety. - Source: PubMed
Braconnier PaulineCharlier MathildeRomanin AlessiaGilbert NicolasDesmet NathalieHermans Emmanuel - Tau protein aggregates adopt distinct conformations across tauopathies, yet the protein interactions engaged by disease-specific polymorphs remain poorly characterized. Here, we demonstrate that conformationally distinct tau polymorphs associate with disease-specific interaction networks across Alzheimer's disease (AD), progressive supranuclear palsy (PSP), and dementia with Lewy bodies (DLB). Interactome profiling of tau aggregates from PBS- and sarkosyl-soluble brain fractions identified 493 high-confidence interactors exhibiting remarkable disease specificity. As an exploratory feature discovery machine learning classification discriminated against diseases using as few as four to six protein features. AD tau selectively engaged glycolytic enzymes, TCA cycle components, and glutamate/GABA cycling machinery, with the astrocytic transporter SLC1A2 showing 27-fold enrichment. PSP tau exhibited extensive interactor depletion alongside selective proteasome enrichment, whereas DLB tau associated with neurogenesis modulators while depleting neuroinflammatory mediators. Interaction patterns were corroborated by parallel reaction monitoring mass spectrometry and proximity ligation assays and corresponded to disease-specific post-translational modification profiles. These findings show that tau polymorph conformations are associated with disease-specific interaction networks, providing molecular insight into tauopathy heterogeneity. - Source: PubMed
Publication date: 2026/08/18
Puangmalai NichaBhatt NemilSuthprasertporn NopparatMiranda-Morales Ernesto GShchankin NikitaSamples MadisonBalci Ahmet ELiew Jia YiMontalbano MauroZhao YingxinKayed Rakez - Opioid addiction is driven by maladaptive reward memory, yet its molecular underpinnings remain poorly understood. Circular RNAs (circRNAs) have emerged as key regulators of neuroplasticity, but their roles in addiction-related memory remain unclear. Here, we identify circUnc79, a neuron-enriched and synaptically localized circRNA, as a critical modulator of morphine reward memory in the medial prefrontal cortex (mPFC). In the morphine-induced conditioned place preference (CPP) model, circUnc79 expression is dynamically downregulated during cue-induced memory retrieval. Gain- and loss-of-function experiments demonstrate that circUnc79 bidirectionally regulates the acquisition and persistence of morphine reward memory, without affecting locomotion, anxiety-like behavior, social interaction, or sucrose reward. Mechanistically, circUnc79 acts as a competing endogenous RNA for miR-149-3p, thereby relieving its repression of excitatory amino acid transporter 2 (EAAT2, encoded by ). Elevated neuronal EAAT2 enhances presynaptic glutamate reuptake and recycling, supporting reward memory encoding. Manipulation of miR-149-3p produces opposite behavioral and synaptic effects, supporting the functional relevance of this regulatory axis. These findings reveal a circUnc79/miR-149-3p/EAAT2 pathway that regulates synaptic plasticity underlying opioid reward memory and highlight circUnc79 as a potential therapeutic target for opioid use disorders. - Source: PubMed
Publication date: 2026/06/08
Yang XixiGao FeifeiYang ZhuojinYu DongyuChen JieYao ZhenLiao QiYang JingsiLiu JunlinGu BoyuanZhang YuxiangYan Chunxia - The preBötzinger complex (preBötC) is a medullary network that generates the inspiratory phase of respiratory rhythm in mammals and depends critically on glutamatergic transmission. To characterize the anatomical organization of excitatory signaling elements within this network, we analyzed the distribution, morphology, and colocalization of the AMPA receptor subunit GluA2 and the NMDA receptor subunit NR1, together with the postsynaptic scaffold protein PSD95. We also used immunofluorescence and confocal microscopy to examine the spatial relationship between GluA2-positive puncta and the astrocytic glutamate transporter EAAT2 in the preBötC of adult male rats. NR1-positive puncta were more abundant and densely distributed than GluA2-positive puncta, whereas GluA2-NR1 colocalized puncta constituted only a small fraction of either receptor population. NR1-positive puncta also showed limited colocalization with PSD95-positive puncta, indicating that a substantial fraction of NR1 immunoreactivity is not associated with PSD95-defined postsynaptic domains under the present imaging conditions. In contrast, GluA2-positive puncta displayed a non-random spatial proximity with EAAT2 astrocytic profiles and were frequently located within submicron distances. Together, these findings reveal a spatially differentiated organization of glutamatergic elements in the preBötC, characterized by abundant non-PSD95-associated NR1-positive puncta and close apposition between GluA2-positive puncta and EAAT2-immunoreactive astrocytic profiles. This organization provides an anatomical framework for future studies testing how glutamate receptor localization and glutamate clearance mechanisms contribute to excitability and respiratory rhythm generation and modulation. - Source: PubMed
Publication date: 2026/08/06
Olmos-Pastoresa Carol AlejandraVázquez-Mendoza EnriqueVázquez-Martínez OliviaLópez-Meraz María LeonorBeltran-Parrazal LuisMorgado-Valle Consuelo - Cerebral malaria (CM) is associated with disruption of the blood-brain barrier (BBB), neurovascular injury, and high mortality. Although mesenchymal stem cells (MSCs) have demonstrated therapeutic efficacy in experimental cerebral malaria (ECM), the molecular mechanisms underlying these effects remain insufficiently defined. In this study, we investigated how MSC treatment modulates host miRNA networks during ECM using a Plasmodium berghei ANKA infection in C57BL/6 mice. MSC treatment significantly reduced clinical severity, improved survival, and preserved BBB integrity, as indicated by decreased Evans blue extravasation and reduced microvascular sequestration within brain. RNA sequencing identified 64 differentially expressed miRNAs associated with MSC treatment. Pathway enrichment using DIANA-miRPath v4.0 identified 23 miRNAs associated to CM-relevant pathways. Eleven miRNAs with highest pathway interactions were subsequently validated by RT-qPCR, confirming consistent down-regulation of eight miRNAs following MSC treatment. miRNA-mRNA network construction revealed several hub genes, including Rora, Nfia, Nfib, Slc1a2, Tcf4, Pura, and Atxn1, linked to neurological phenotypes relevant to CM pathology. Collectively, these findings suggest that MSCs mitigate ECM pathology by reprogramming miRNA-mRNA regulatory networks governing cerebral and neuronal stability. The identified miRNA-mRNA hubs represent promising candidates for future biomarker studies and may provide a foundation for the development of adjunctive therapeutic strategies against cerebral malaria. - Source: PubMed
Publication date: 2026/07/07
Chaudhary AmrendraSharma InduThakur Reva SharanRanjha RiteshDas Jyoti