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Merck
CN

MAB5578

抗-NMDAR2D抗体

ascites fluid, clone 1G9.39A5, Chemicon®

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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-NMDAR2D抗体, ascites fluid, clone 1G9.39A5, Chemicon®

biological source

mouse

conjugate

unconjugated

antibody form

ascites fluid

clone

1G9.39A5, monoclonal

species reactivity

human, mouse, rat, rabbit

manufacturer/tradename

Chemicon®

technique(s)

western blot: suitable

isotype

IgG2b

NCBI accession no.

UniProt accession no.

shipped in

dry ice

target post-translational modification

unmodified

Quality Level

Gene Information

human ... GRIN2D(2906)

Analysis Note

对照
大鼠前脑或小脑。

Application

抗NMDAR2D抗体检测NMDAR2D水平,&已发布&验证可用于WB。
研究子类别
神经递质&受体
研究类别
神经科学
蛋白质印迹:针对大鼠脑裂解物为1:500-1:1,000。

最佳工作稀释度必须由最终使用者进行确定。

Biochem/physiol Actions

NMDAR2D,C末端。通过蛋白质印迹法,抗体与约145的弱条带反应。根据所用样品和抗体浓度,可观察到约75 kDa的额外条带。

Disclaimer

除非我们的目录或产品随附的其他公司文件中另有说明,否则我们的产品预期仅用于研究用途,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对人类或动物的任何类型的消费或应用。

Immunogen

来自大鼠NMDAR2D的重组蛋白。

Physical form

液体。

Preparation Note

接收后,以未稀释的等分试样在-20°C下保存长达6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

10 - Combustible liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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Sharon A Swanger et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 35(48), 15971-15983 (2015-12-04)
The GluN2D subunit of the NMDA receptor is prominently expressed in the basal ganglia and associated brainstem nuclei, including the subthalamic nucleus (STN), globus pallidus, striatum, and substantia nigra. However, little is known about how GluN2D-containing NMDA receptors contribute to
Gajanan P Shelkar et al.
Scientific reports, 9(1), 7572-7572 (2019-05-22)
The GluN2C- and GluN2D-containing NMDA receptors are distinct from GluN2A- and GluN2B-containing receptors in many aspects including lower sensitivity to Mg2+ block and lack of desensitization. Recent studies have highlighted the unique contribution of GluN2C and GluN2D subunits in various
Marie A Doyle et al.
Neuropharmacology, 225, 109377-109377 (2022-12-18)
Stress coping strategies represent critical responses to environmental challenges, and active coping has been linked to stress resilience in humans. Understanding the neuroadaptations that support these strategies may provide insights into adaptive and maladaptive stress responses. NMDA receptors (NMDARs) play
H Wang et al.
Neuroscience, 188, 168-181 (2011-05-21)
Untimely activation of nicotinic acetylcholine receptors (nAChRs) by nicotine results in short- and long-term consequences on learning and behavior. In this study, the aim was to determine how prenatal nicotine exposure affects components of glutamatergic signaling in the hippocampus during
Riley E Perszyk et al.
Molecular pharmacology, 90(6), 689-702 (2016-11-03)
N-methyl-d-aspartate receptors (NMDARs) are ionotropic glutamatergic receptors that have been implicated in learning, development, and neuropathological conditions. They are typically composed of GluN1 and GluN2A-D subunits. Whereas a great deal is known about the role of GluN2A- and GluN2B-containing NMDARs

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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