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Merck
CN

MAB5216

抗-NMDAR2A抗体

Chemicon®, from mouse

别名:

NR2A

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关于此项目

UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
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产品名称

抗-NMDAR2A抗体, Chemicon®, from mouse

biological source

mouse

conjugate

unconjugated

antibody form

affinity purified immunoglobulin

clone

monoclonal

species reactivity

human

manufacturer/tradename

Chemicon®

technique(s)

immunocytochemistry: suitable
immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable
western blot: suitable

isotype

IgG1

NCBI accession no.

UniProt accession no.

shipped in

dry ice

target post-translational modification

unmodified

Quality Level

Gene Information

human ... GRIN2A(2903)

Application

在4%多聚甲醛&0.125%戊二醛固定的组织上进行免疫组化(轻和EM):2.5-5 μg/mL。

免疫细胞化学:2.5-5.0μg/mL

蛋白质印迹:1-5 μg/mL 最佳工作稀释度必须由最终用户进行确定。
抗i-NMDAR2A抗体可检测i-NMDAR2A的水平& 已有相关文献发表 &经验证可用于IH(P)、IC、IH & WB。
研究子类别
神经递质 & 受体
研究类别
神经科学

Disclaimer

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。

Immunogen

由人NMDAR2A 的氨基酸区域1099-1213产生的GST融合蛋白。

Other Notes

替代:MAB5218
浓度:请参考批次特异性浓缩物的检验报告。

Physical form

亲和纯化的免疫球蛋白。 溶于PBS中的液体。不含防腐剂。
形式:纯化

Preparation Note

以未稀释的等分试样在-20°C下冷冻保存长达12 个月。应避免反复冻/融循环。

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

存储类别

12 - Non Combustible Liquids

wgk

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable


分析证书(COA)

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Regulation of NMDA receptors by cyclin-dependent kinase-5.
Li, BS; Sun, MK; Zhang, L; Takahashi, S; Ma, W; Vinade, L; Kulkarni, AB; Brady, RO; Pant, HC
Proceedings of the National Academy of Sciences of the USA null
Andre Fischer et al.
Neuron, 48(5), 825-838 (2005-12-13)
While deregulation of cyclin-dependent kinase 5 (Cdk5) has been implicated in neurodegenerative diseases, its precise role in synaptic plasticity and memory remains elusive. Proteolytic cleavage of p35, a regulatory subunit of Cdk5, by calpain results in the generation of the
Céline Bidoret et al.
Frontiers in synaptic neuroscience, 7, 1-1 (2015-03-10)
N-methyl-D-aspartate receptors (NMDARs) in cerebellar molecular layer interneurons (MLIs) are expressed and activated in unusual ways: at parallel fibre (PF) synapses they are only recruited by repetitive stimuli, suggesting an extrasynaptic location, whereas their activation by climbing fibre is purely
Ruifa Mi et al.
Neuron, 44(2), 335-349 (2004-10-12)
Under standard conditions, cultured ventral spinal neurons cluster AMPA- but not NMDA-type glutamate receptors at excitatory synapses on their dendritic shafts in spite of abundant expression of the ubiquitous NMDA receptor subunit NR1. We demonstrate here that the NMDA receptor
Sylvie L Lesuis et al.
Neuropharmacology, 149, 195-203 (2019-01-15)
Programming of the brain by early life stress has been associated with alterations in structure and function of the dorsal hippocampus. Yet, the underlying molecular mechanisms remain largely elusive. In this study, we examined the effects of early life stress

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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