SLC1A2 antibody - N-terminal region (ARP33840_P050)
- Known as:
- SLC1A2 (anti-) - N-terminal region (ARP33840_P050)
- Catalog number:
- arp33840_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SLC1A2 antibody - N-terminal region (ARP33840_P050)
Related genes to: SLC1A2 antibody - N-terminal region (ARP33840_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 - N-terminal region (ARP33840_P050)
Related articles to: SLC1A2 antibody - N-terminal region (ARP33840_P050)
- 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 - Scotopic vision impairment as an early event is found in diabetic retinopathy. However, the underlying mechanisms behind hyperglycemia-induced scotopic vision impairment remain unclear. This study aims to identify that Grm6 is associated with glutamate accumulation-induced scotopic vision impairment under hyperglycemia. - Source: PubMed
Publication date: 2025/11/10
Lian YingZhao YanpuYang XiaoyuHe HongjieYang ZhanyiZhang HuanhuanYan GuigangLu LuMi JiaTian GengZhu Yanping - This study investigated the expression of NDNF and SLC1A2 in the dorsolateral prefrontal cortex of individuals with Autism Spectrum Disorder (ASD), a region linked to executive functions, emotional regulation, social skills, and sensory processing. - Source: PubMed
Publication date: 2026/02/16
de Andrade Ariel Moraesde Souza Larysy Raquelly VidalOliveira Rodrigo FreirePaiva Karina MaiaFiuza Felipe Portode Farias Pedro Henrique Silvada Silva Júnior Roque RibeiroHolanda Maria Vanessa Freitasde Medeiros Fernandes Thales Allyrio Araújode Góis Morais Paulo Leonardo Araújode Paiva Cavalcanti José Rodolfo Lopes - Semantic variant of primary progressive aphasia is a clinical subtype of frontotemporal lobar degeneration and is marked by TDP-43 subtype C pathology (FTLD-TDP C). It is a sporadic disease, yet has a strikingly homogeneous clinicopathological presentation, suggesting a common pathophysiology. The aim of this study was to discover dysregulated pathways in FTLD-TDP C through transcriptomics of the temporal cortex, its most affected region. Bulk RNA sequencing was conducted on temporal cortices of a post-mortem cohort of 18 FTLD-TDP C patients and 23 sex- and age-matched controls. Differential expression and functional analyses were run to detect differentially expressed genes with FDR<0.05 (DEG) and functionally annotate them. We assessed enrichment of TARDBP's protein interactors and RNA targets in DEG. Our findings were compared to other published RNA sequencing data of tauopathies (Alzheimer's dementia, progressive supranuclear palsy and FTLD with MAPT), FTLD-TDP (subtypes A&B) and available proteomics of this cohort. Furthermore, we performed weighted gene co-expression network analysis (WGCNA). We adjusted for differences in cell type composition between cases and controls using cell deconvolution, and removed genes dysregulated in temporal cortices of other datasets. In DEG of FTLD-TDP we focused on enrichment of synaptic processes using SynGO. We found upregulation of damage response, cell structure, RNA splicing processes and downregulation of synaptic processes in 6322 DEG and five disease-related WGCNA modules. TARDBP-related genes were enriched in DEG. Additionally, transmembrane transport across the neurovascular unit was dysregulated. After cell deconvolution and removal of common tau-genes, postsynaptic processes remained dysregulated, specifically gene ontology terms 'modulation of chemical synaptic transmission' and 'neurotransmitter receptor localisation to postsynaptic specialisation membrane'. We found eleven synaptic FTLD-TDP C-specific genes affected on both RNA- and protein-level in the temporal cortex, which were involved in synaptic adhesion (CADM1, NCAN), signal transmission (COMT, RGS144, SLC1A2, TUBB2B) and synaptic plasticity (BEGAIN, ITPKA, LRFN1, RAB3B, SYNPO). In conclusion, a wide range of processes were dysregulated on RNA-level in the temporal cortex of FTLD-TDP C, including commonly affected processes in neurodegeneration, such as structural cell alterations. Dysregulation of TARDBP-related genes and RNA splicing has also been observed in other TDP-43 proteinopathies. Importantly, we found that postsynaptic processes were downregulated in FTLD-TDP C, after removing tauopathy-related genes and after cell deconvolution. In particular, assembly of receptors at the postsynaptic membrane and synaptic signal transmission were affected, both on RNA and protein level. Future research on these pathways could elucidate distinct pathophysiological mechanisms and guide targeted clinical approaches. - Source: PubMed
Publication date: 2026/03/06
Rajicic AnaMol Merel OMelhem ShamiramKisic Helenavan Swieten John CSeelaar Harrovan Rooij Jeroen G J