生物来源
rabbit
质量水平
抗体形式
affinity isolated antibody
抗体产品类型
primary antibodies
克隆
polyclonal
纯化方式
affinity chromatography
种属反应性
human, mouse, rat
技术
immunohistochemistry: suitable (paraffin)
western blot: suitable
NCBI登记号
UniProt登记号
运输
wet ice
靶向翻译后修饰
unmodified
基因信息
human ... GRIA1(2890)
mouse ... Gria1(14799)
rat ... Gria1(50592)
一般描述
谷氨酸受体（GluRs）是一个多样化的群体，负责介导脊椎动物中枢神经系统中的大多数兴奋性突触传递。它们可以分为离子型或代谢型，并可再根据其激动剂的偏好型（NMDA、AMPA或红藻氨酸）而进一步分类。存在有四种类型的AMPA选择性GluR亚基（GluR1、GluR2、GluR3和GluR4）。不同亚基的四聚体或五聚体组合有助于AMPA受体的功能多样性。AMPA受体可在大多数兴奋性突触中介导快速突触电流，具有以亚型组成为特征的化学计量。控制钙渗透性的关键残基位于孔环区域。在GluR1、GluR3和GluR4中，该位置被一个Gln残基所占据。从突触后膜插入或去除GluR1/GluR4寡聚通道似乎是LTP/LTD活性依赖性的，而GluR2/GluR3寡聚体不断循环。
特异性
该抗体识别GluR1的胞外域。
免疫原
对应于大鼠GluR1胞外域的KLH偶联线性肽。
应用
免疫组化分析：代表性批次的1：1,000 的稀释液在人大脑和人小脑组织中检测到GluR1。
抗GluR1抗体是一种高度特异性的兔多克隆抗体，其靶向GluR1&已在蛋白质印迹& IHC（石蜡）中进行了测试。
质量
通过蛋白质印迹对大鼠脑组织裂解液进行了评估。
蛋白质印迹分析：2.0 µg/mL该抗体在10 µg大鼠脑组织裂解液中检测到GluR1。
蛋白质印迹分析：2.0 µg/mL该抗体在10 µg大鼠脑组织裂解液中检测到GluR1。
目标描述
观察值〜110 kDa
联系
替代品：PC246-100UG
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WGK
WGK 1
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Jennifer L Sanderson et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 38(11), 2863-2876 (2018-02-15)
Neuronal information processing requires multiple forms of synaptic plasticity mediated by NMDARs and AMPA-type glutamate receptors (AMPARs). These plasticity mechanisms include long-term potentiation (LTP) and long-term depression (LTD), which are Hebbian, homosynaptic mechanisms locally regulating synaptic strength of specific inputs
Núria Martín-Flores et al.
Cell death & disease, 11(7), 569-569 (2020-08-01)
RTP801/REDD1 is a stress-responsive protein that mediates mutant huntingtin (mhtt) toxicity in cellular models and is up regulated in Huntington's disease (HD) patients' putamen. Here, we investigated whether RTP801 is involved in motor impairment in HD by affecting striatal synaptic
Tao Wu et al.
Journal of biomedical science, 26(1), 79-79 (2019-10-21)
Neuronal activity-induced changes in gene expression patterns are important mediators of neuronal plasticity. Many neuronal genes can be activated or inactivated in response to neuronal depolarization. Mechanisms that activate gene transcription are well established, but activity-dependent mechanisms that silence transcription
Katherine J Sellers et al.
Alzheimer's & dementia : the journal of the Alzheimer's Association, 14(3), 306-317 (2017-10-23)
Synapse loss is the structural correlate of the cognitive decline indicative of dementia. In the brains of Alzheimer's disease sufferers, amyloid β (Aβ) peptides aggregate to form senile plaques but as soluble peptides are toxic to synapses. We previously demonstrated
Dipen Rajgor et al.
Cell reports, 31(12), 107785-107785 (2020-06-25)
Molecular mechanisms underlying plasticity at brain inhibitory synapses remain poorly characterized. Increased postsynaptic clustering of GABAA receptors (GABAARs) rapidly strengthens inhibition during inhibitory long-term potentiation (iLTP). However, it is unclear how synaptic GABAAR clustering is maintained to sustain iLTP. Here
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