2008年9月9日 · To accomplish this we used a recombinant adeno-associated virus vector, AAV1–glial fibrillary acidic protein (GFAP)–EAAT2, designed to selectively drive the overexpression of EAAT2 within astrocytes.

谷氨酸的稳态主要受兴奋性氨基酸转运蛋白 (EAAT) 调节，尤其是星形胶质细胞中的 EAAT2。 由 EAAT2 功能障碍或失调引起的突触间隙谷氨酸过多可导致兴奋性毒性、神经元死亡和认知功能障碍。 然而，星形胶质细胞EAAT2表达和功能的详细调控机制尚不清楚。 在这项研究中，首先，我们发现 YAP GFAP -CKO 小鼠（有条件地敲除星形胶质细胞中的 Yes 相关蛋白 [YAP]）的神经元死亡和认知功能受损增加，并通过 RNA 测序将 EAAT2 鉴定为 YAP 的下游靶标。 其次，EAAT2 …

To accomplish this we used a recombinant Adeno-associated virus vector, AAV1-GFAP-EAAT2, designed to selectively drive the overexpression of EAAT2 within astrocytes. Both viral mediated gene delivery and β-lactam antibiotic (penicillin-G) treatment of rat hippocampal slice cultures resulted in a significant increase in both the expression of ...

The excitatory amino acid transporter 2 (EAAT2) is the dominant glutamatergic transporter in the human brain, responsible for efficient removal of glutamate from the synaptic cleft for recycling within glial cells. As such, it has a key role in maintaining excitatory-inhibitory homeostasis.

Excitatory amino acid transporter (EAAT) 1 and EAAT2 are Na + -dependant glutamate transporters expressed predominantly in glia cells of the central nervous system. As the most abundant glutamate transporters, their primary role is to modulate levels of glutamatergic excitability and prevent spill over of glutamate beyond the synapse.

In this study, first, we found increased neuronal death and impairment of cognitive function in YAP GFAP-CKO mice (conditionally knock out Yes-associated protein [YAP] in astrocytes), and identified EAAT2 as a downstream target of YAP through RNA sequencing.

2008年9月9日 · To accomplish this we used a recombinant adeno-associated virus vector, AAV1-glial fibrillary acidic protein (GFAP)-EAAT2, designed to selectively drive the overexpression of EAAT2 within astrocytes.

2014年2月24日 · Glial glutamate transporter EAAT2 plays a major role in glutamate clearance in synaptic clefts. Several lines of evidence indicate that strategies designed to increase EAAT2 expression have potential for preventing excitotoxicity, which contributes to neuronal injury and death in neurodegenerative diseases.

Dual immunofluorescence labeling of ET cerebellar cortex with anti-EAAT1 or anti-EAAT2 (Alexa 488, green, A, D, G, J, M, P), anti-GFAP (Alexa 594, red, B, E, K, Q), and anti-glutamate...

Excitatory amino acid transporter 2 (EAAT2) is primarily responsible for clearance of extracellular glutamate to prevent neuronal excitotoxicity and hyperexcitability. EAAT2 plays a critical role in regulation of synaptic activity and plasticity. In addition, EAAT2 has been implicated in the pathogenesis of many central nervous system disorders.