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Merck
CN

MAB2263

Sigma-Aldrich

抗GluR1-NT(NT)抗体,克隆RH95

clone RH95, from mouse

别名:

AMPA 1, AMPA-selective glutamate receptor 1, Glutamate receptor ionotropic, AMPA 1, glutamate receptor, ionotropic, AMPA 1

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关于此项目

UNSPSC代码:
12352203
eCl@ss:
32160702
NACRES:
NA.41
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生物来源

mouse

质量水平

偶联物

unconjugated

抗体形式

purified immunoglobulin

抗体产品类型

primary antibodies

克隆

RH95, monoclonal

种属反应性

rat

技术

ELISA: suitable
immunocytochemistry: suitable
immunoprecipitation (IP): suitable
western blot: suitable

同位素/亚型

IgG2aκ

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)

一般描述

110kda
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。

免疫原

在N末端周围设计的大鼠GluR1的甲状腺球蛋白结合的线性肽。
表位:N末端

应用

抗GluR1-NT(N-末端)抗体,克隆RH95是针对GluR1-NT(N-末端)的抗体,用于WB,IP,IC,ELISA。
研究子类别
神经递质& 受体
研究类别
神经科学

生化/生理作用

该抗体识别N-末端的GluR1。

外形

形式:纯化
纯化的小鼠单克隆IgG2aκ,溶于含有0.1 M Tris-甘氨酸(pH 7.4,150 mM NaCl)和0.05%叠氮化钠的缓冲液中。
纯化的蛋白G

制备说明

自收到之日起,在 2-8°C 条件下可稳定保存1年

分析说明

对照
小鼠脑裂解物
已通过蛋白质印迹在大鼠脑裂解物中进行了评估。

蛋白质印迹分析:该抗体以 1:1000 的稀释度在 10 µg 大鼠脑裂解物中检测到 GluR1。

其他说明

浓度:请参考批次特异性浓缩物的分析证书。

免责声明

除非我们的产品目录或产品附带的其他公司文档另有说明,否则我们的产品仅供研究使用,不得用于任何其他目的,包括但不限于未经授权的商业用途、体外诊断用途、离体或体内治疗用途或任何类型的消费或应用于人类或动物。

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储存分类代码

12 - Non Combustible Liquids

WGK

WGK 1

闪点(°F)

Not applicable

闪点(°C)

Not applicable


分析证书(COA)

输入产品批号来搜索 分析证书(COA) 。批号可以在产品标签上"批“ (Lot或Batch)字后找到。

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在文件库中查找您最近购买产品的文档。

访问文档库

PKM? knockdown disrupts post-ischemic long-term potentiation via inhibiting postsynaptic expression of aminomethyl phosphonic acid receptors.
Cheng, N; Hu, X; Tian, T; Lu, W
Journal of biomedical research null
Xiaofen Zhong et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 32(37), 12841-12847 (2012-09-14)
MeCP2 (methyl CpG binding protein 2) is a key player in recognizing methylated DNA and interpreting the epigenetic information encoded in different DNA methylation patterns. The functional significance of MeCP2 to the mammalian nervous system is highlighted by the discovery
Caroline Jung et al.
Psychopharmacology, 233(17), 3161-3172 (2016-07-05)
When ad libitum-fed rats undergo cocaine place preference conditioning (CPP) but are switched to food restriction for testing, CPP becomes resistant to extinction and correlates with phosphorylation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor GluA1 at Ser845 in nucleus accumbens (NAc) core.
Impaired spatial memory and enhanced long-term potentiation in mice with forebrain-specific ablation of the Stim genes.
Garcia-Alvarez, G; Shetty, MS; Lu, B; Yap, KA; Oh-Hora, M; Sajikumar, S; Bichler, Z; Fivaz, M
Frontiers in Behavioral Neuroscience null
Paul Farrow et al.
eLife, 4, e09693-e09693 (2015-12-02)
AMPA receptor (AMPAR) function is modulated by auxiliary subunits. Here, we report on three AMPAR interacting proteins-namely CKAMP39, CKAMP52 and CKAMP59-that, together with the previously characterized CKAMP44, constitute a novel family of auxiliary subunits distinct from other families of AMPAR

相关内容

Glutamate is an excitatory neurotransmitter found in the synaptic vesicles of glutamatergic synapses. The post-synaptic neurons in these synapses contain ionotropic and metabotropic glutamate receptors. Glutamate binds to AMPA (α-amino-3-hydroxy-5- methylisoxazole-4-propionic acid) subtype glutamate receptors, leading to sodium influx into the post-synaptic cell and resulting in neuronal excitability and synaptic transmission. The NMDA (N-methyl-d-aspartate) subtype glutamate receptors, on the other hand, regulate synaptic plasticity, and can influence learning and memory. The metabotropic g-protein coupled mGluRs modulate downstream calcium signaling pathways and indirectly influence the synapse’s excitability. The synaptic architecture includes intracellular scaffolding proteins (PSD-95, GRIP), intercellular cell adhesion molecules (NCAMs, N-Cadherins), and a variety of signaling proteins (CaMKII/PKA, PP1/PP2B). Processes critical for synaptic transmission and plasticity are influenced by these molecules and their interactions. When the function of these molecules is disrupted, it leads to synaptic dysfunction and degeneration, and can contribute to dementia as seen in Alzheimer’s disease.

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