Eaat4,Excitatory amino acid transporter 4,High-affinity neuronal glutamate transporter,Mouse,Mus musculus,Slc1a6,Sodium-dependent glutamate_aspartate transporter,Solute carrier family 1 member 6
- Known as:
- Eaat4,Excitatory amino acid transporter 4,High-antigenic neuronal glutamate transporter,Mouse,Mus musculus,Slc1a6,Sodium-dependent glutamate_aspartate transporter,Solute carrier family 1 member 6
- Catalog number:
- EIAAB12307
- Category:
- -
- Supplier:
- EIAab
- Gene target:
- Eaat4 Excitatory amino acid transporter 4 High-affinity neuronal glutamate Mouse Mus musculus Slc1a6 Sodium-dependent glutamate_aspartate Solute carrier family 1 member 6
Related genes to: Eaat4,Excitatory amino acid transporter 4,High-affinity neuronal glutamate transporter,Mouse,Mus musculus,Slc1a6,Sodium-dependent glutamate_aspartate transporter,Solute carrier family 1 member 6
- Gene:
- SLC1A6 NIH gene
- Name:
- solute carrier family 1 member 6
- Previous symbol:
- -
- Synonyms:
- EAAT4
- Chromosome:
- 19p13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-05
- Date modifiied:
- 2016-02-17
Related products to: Eaat4,Excitatory amino acid transporter 4,High-affinity neuronal glutamate transporter,Mouse,Mus musculus,Slc1a6,Sodium-dependent glutamate_aspartate transporter,Solute carrier family 1 member 6
Related articles to: Eaat4,Excitatory amino acid transporter 4,High-affinity neuronal glutamate transporter,Mouse,Mus musculus,Slc1a6,Sodium-dependent glutamate_aspartate transporter,Solute carrier family 1 member 6
- The search for biomarkers to predict radiosensitivity is important not only to individualize radiotherapy of cancer patients but also to forecast radiation exposure risks. The aim of this study was to devise a machine-learning method to stratify radiosensitivity and to investigate its association with genome-wide copy number variations (CNVs) as markers of sensitivity to ionizing radiation. - Source: PubMed
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Li JinnaGuo QingXing Rui - The purpose of this study was to identify the ferroptosis-related molecular subtypes in muscle invasive bladder cancer (MIBC) associated with the tumor microenvironment (TME) and immunotherapy. - Source: PubMed
Wang HaojieDai YingboWu XiangHu BowenWang ZiYan Minbo - Low-grade dysembryoplastic neuroepithelial tumors (DNTs) are a frequent cause of drug-refractory epilepsy. Molecular mechanisms underlying seizure generation in these tumors are poorly understood. This study was conducted to identify altered genes in nonneoplastic epileptogenic cortical tissues (ECTs) resected from DNT patients during electrocorticography (ECoG)-guided surgery. RNA sequencing (RNAseq) was used to determine the differentially expressed genes (DEGs) in these high-spiking ECTs compared to non-epileptic controls. A total of 477 DEGs (180 upregulated; 297 downregulated) were observed in the ECTs compared to non-epileptic controls. Gene ontology analysis revealed enrichment of genes belonging to the following Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways: (i) glutamatergic synapse; (ii) nitrogen metabolism; (iii) transcriptional misregulation in cancer; and (iv) protein digestion and absorption. The glutamatergic synapse pathway was enriched by DEGs such as GRM4, SLC1A6, GRIN2C, GRM2, GRM5, GRIN3A, and GRIN2B. Enhanced glutamatergic activity was observed in the pyramidal neurons of ECTs, which could be attributed to altered synaptic transmission in these tissues compared to non-epileptic controls. Besides glutamatergic synapse, altered expression of other genes such as GABRB1 (synapse formation), SLIT2 (axonal growth), and PROKR2 (neuron migration) could be linked to epileptogenesis in ECTs. Also, upregulation of GABRA6 gene in ECTs could underlie benzodiazepine resistance in these patients. Neural cell-type-specific gene set enrichment analysis (GSEA) revealed transcriptome of ECTs to be predominantly contributed by microglia and neurons. This study provides first comprehensive gene expression profiling of nonneoplastic ECTs of DNT patients and identifies genes/pathways potentially linked to epileptogenesis. - Source: PubMed
Publication date: 2022/05/28
Kumar KrishanBanerjee Dixit AparnaTripathi ManjariDubey VivekSiraj FouziaSharma Mehar ChandLalwani SanjeevChandra P SaratBanerjee Jyotirmoy - Cadmium (Cd) is a toxic heavy metal that can facilitate the development and progression of breast cancer (BC). Emerging evidence has indicated that the progression of Cd-exposed BC is related to the dysregulation of microRNAs (miRNAs). The purpose of our study was to investigate the expression pattern and underlying mechanisms of miR-374c-5p in Cd-mediated BC progression. In this study, T-47D cells and MCF-7 cells were treated with different concentrations of Cd (0.1, 1 and 10 μM) for 72 h. MiR-374c-5p expression was downregulated, and transfection of miR-374c-5p mimics significantly decreased BC cell proliferation, migration and invasion induced by 10 μM Cd. Importantly, we used the Cytoscape software plugin cytoHubba to analyse the intersected genes between our RNA-Seq results and the mirDIP database, and six hub genes (CNR1, CXCR4, GRM3, RTN1, SLC1A6 and ZEB1) were identified as potential direct targets of miR-374c-5p in our model; however, luciferase reporter assays indicated that miR-374c-5p only repressed GRM3 by directly binding to its 3'-untranslated region (UTR). Of note, we verified that suppression of N6-methyladenosine (m6A) modification led to miR-374c-5p downregulation by decreasing its RNA transcript stability. Together, these findings demonstrated that m6A modification of pri-miRNA-374c blocks miRNA-374c-5p maturation and then activates GRM3 expression, which drives BC cell metastasis after Cd exposure. - Source: PubMed
Publication date: 2021/12/15
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