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)
- Glutamate spillover from excitatory synapses modulates neighboring inhibitory synapses, yet the ultrastructural organization of the major glutamate transporter GLT-1 at these sites remains poorly defined. Using quantitative pre-embedding electron microscopy in rat and human cortex, we found that GLT-1-positive astrocytic leaflets (ALs) were frequently juxtaposed to morphologically identified symmetric synapses, with similar prevalence across axo-somatic, proximal axo-dendritic, and distal axo-dendritic subtypes. Because inhibitory synapses are embedded in a dense excitatory neuropil, we applied distance-based phenotyping relative to the nearest asymmetric synapse to define symmetric-associated GLT-1+ ALs. Within this population, distal axo-dendritic symmetric synapses showed shorter AL-to-synaptic-edge distances and were embedded in a tighter local excitatory microenvironment. Post-embedding immunogold further showed that GLT-1 was enriched at the plasma membranes of ALs and localized extrasynaptically relative to symmetric synapses. Consistently, symmetric-associated membrane GLT-1 and closely spaced GLT-1/α2 couples (with an interdistance ≤ 50 nm) were preferentially localized within 1000 nm of distal symmetric synapses compared to proximal. Similar organizational features of membrane GLT-1/α2 couples were observed in human cortex. These findings identify a subtype-dependent extrasynaptic astrocytic GLT-1 organization at cortical inhibitory synapses and provide a morphological framework for glutamate-dependent modulation of inhibitory signaling. - Source: PubMed
Melone MarcelloDi Palma MichaelScimemi AnnalisaConti Fiorenzo - Traumatic brain injury (TBI) is a significant health problem around the world. Even mild TBI (mTBI) can cause long-term neurodegenerative consequences such as Alzheimer's disease. Excitotoxicity plays a vital role in neuronal death after TBI, and Glutamate Transporter 1 (GLT-1) may be a therapeutic target for reducing TBI outcomes. It has been found that ceftriaxone (a beta-lactam antibiotic) can reduce TBI symptoms, including astrocyte reactivity and inflammation, and may also affect GLT-1 expression. The primary objective of this study is to investigate how ceftriaxone affects GLT-1 in neurons and astrocytes. mTBI was modelled in male albino mice using a modified Marmarou's weight-drop method. Ceftriaxone (250 mg/kg) was administered intraperitoneally for 3 and 5 days after injury. We immunolabeled coronal brain slices to detect GLT-1 expression and distribution, using antibodies to Glial Fibrillary Acidic Protein (GFAP - astrocytic marker), NeuN (neuronal marker), and GLT-1. The presence of fluorescently labelled areas and the ratio of fluorophores within each area were examined using an image processing plugin that identifies regions with substantial staining in confocal microscopy images. In this article, we address the dynamics of changes in fluorescence intensity and area for the regions we describe as GFAP, NeuN, and GLT-1. We found that GLT-1 dynamics change in both neurons and astrocytes following mTBI, but ceftriaxone affects these changes. In our opinion, due to the displacement of glutamate transporter clusters in cells, they cannot properly fulfil their function of limiting excitability produced by trauma. - Source: PubMed
Publication date: 2026/05/08
Naumenko YanaOlifirov BorysYuryshynets IradaPivneva Tetyana - Recurrent miscarriage (RM), a complex pregnancy disorder with largely undefined molecular mechanisms, has been associated with epigenetic abnormalities in chorionic tissue. This study aimed to elucidate methylation-dependent cilia-related genes (CRGs) implicated in RM. An integrative analysis combining RNA sequencing, public transcriptome data, and DNA methylation profiles was conducted to identify RM-related CRGs. Machine learning algorithms were applied to determine the most relevant candidates. Immune infiltration profiling, gene set enrichment analysis (GSEA), and competitive endogenous RNA (ceRNA) network construction were employed to clarify molecular pathways. RT-qPCR validation was performed using clinical samples. Fourteen methylation-regulated CRGs were identified, among which SLC1A2 and ZDHHC20 were confirmed as key candidates. GSEA indicated their association with spliceosome, cell cycle, and proteasome pathways. Immune analysis demonstrated decreased infiltration of activated CD4 T cells, effector memory CD4 T cells, and Th2 cells in RM, with SLC1A2 and ZDHHC20 expression positively correlated with these immune subsets. The ceRNA networks indicated that SLC1A2 and ZDHHC20 were modulated by 7 miRNAs and 19 lncRNAs, respectively. RT-qPCR results showed significant overexpression of SLC1A2, but not ZDHHC20, in RM chorionic tissue. Collectively, SLC1A2 represents a methylation-regulated CRG that links ciliary impairment, immune imbalance, and epigenetic modulation in RM, revealing a novel molecular axis and suggesting its diagnostic and therapeutic potential. - Source: PubMed
Publication date: 2026/05/09
Li JingJing JunningLiu JingtingZhang DengcaiZhang LiyuanXie Guangmei - Astrocytes play a key role in neuronal homeostasis and in various neural disorders. The generation of astrocytes from neural progenitor cells (NPCs) and its functions are under a complex control of several signaling networks and transcription factors. In this study, we demonstrate that the transcription factor, GLIS similar 3 (GLIS3), which has been implicated in several neurodegenerative diseases, is highly expressed in astrocytes, and is required for the efficient differentiation of human NPCs into astrocytes. Loss of GLIS3 function greatly impairs astrocytes differentiation, resulting in reduced expression of astrocyte markers, whereas expression of exogenous GLIS3 restores the induction of astrocyte specific genes indicating a critical role for GLIS3 in astrocyte differentiation. Integrated transcriptomic and cistromic analyses revealed that GLIS3 directly regulates the transcription of several astrocyte-associated genes, including , , , and , in coordination with lineage-determining factors, such as STAT3, NFIA, and SOX9. We hypothesize that GLIS3 dysfunction disrupts this transcriptional network thereby contributing to astrocyte-associated neurological disorders. Identification of GLIS3 as a key regulator of astrocyte differentiation and gene expression will advance our understanding of its role in neurodegenerative diseases and may provide a new therapeutic target. - Source: PubMed
Publication date: 2026/04/04
Pradhan TapasKang Hong SoonJeon KilsooGrimm Sara APark Kye-YoonJetten Anton M - As the largest white matter tract within the central nervous system (CNS) to connect two cerebral hemispheres, the corpus callosum axon bundle consists of a mixture of myelinated and unmyelinated axons and plays a crucial role in executing sensory, motor and cognitive functions within the CNS. In this study, we comprehensively characterized progressive alterations in myelination and oligodendrocyte lineage cell densities during the postnatal myelin development and then correlated these structural dynamics to the maturation of axonal impulse conduction within the mouse corpus callosum. In addition, we found that the extracellular spaces between callosal axons were significantly reduced during the first three postnatal weeks in mice, while micron-scale diffusion of small molecule within this region remained largely unaffected and displayed isotropy. However, the glutamate transporter GLT-1 was markedly upregulated within the first 3 postnatal weeks, and its expression was found not only in astrocytes but also in oligodendrocyte lineage cells. Finally, we showed that the ectopic callosal axonal vesicle machinery were not fully matured until the later state of myelin development. In summary, our study provided a dynamic profile of the structural and functional maturation of mouse corpus callosum during postnatal myelin development. - Source: PubMed
Johnson HayesBeall MarenLatifi SophiaPeng JuanSun Wenjing