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Merck
CN

04-921

抗-GluR6/7抗体,克隆NL9,兔单克隆

culture supernatant, clone NL904, Upstate®

别名:

Anti-EAA4, Anti-GLR6, Anti-GLUK6, Anti-GLUR6, Anti-GluK2, Anti-MRT6, Anti-NEDLAS

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关于此项目

UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Conjugate:
unconjugated
Clone:
NL904, monoclonal
Application:
immunoprecipitation (IP)
western blot
Species reactivity:
mouse, rat, human
Citations:
37
Technique(s):
immunoprecipitation (IP): suitable
western blot: suitable
Uniprot accession no.:
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产品名称

抗-GluR6/7抗体,克隆NL9,兔单克隆, culture supernatant, clone NL904, Upstate®

biological source

rabbit

conjugate

unconjugated

antibody form

culture supernatant

antibody product type

primary antibodies

clone

NL904, monoclonal

species reactivity

mouse, rat, human

manufacturer/tradename

Upstate®

technique(s)

immunoprecipitation (IP): suitable
western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

dry ice

target post-translational modification

unmodified

Quality Level

Gene Information

human ... GRIK2(2898)

Analysis Note

对照
小鼠脑组织、大鼠脑微粒体制剂、人脑裂解液
已通过免疫印迹分析进行常规评估。

Application

抗GluR6/7抗体,克隆NL9,是一种针对GluR6/7抗体,可用于IP & WB。
研究子类别
神经递质 & 受体
研究类别
神经科学

Biochem/physiol Actions

可识别GluR6/7。

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。

General description

115 kDa

Immunogen

KLH偶联的合成肽,对应于大鼠GluR6的氨基酸894-908(C端)。 免疫序列在人中是相同的。

Other Notes

替代:05-921

Physical form

Preparation Note

自收到之日起在-20°C可稳定保存2年。避免反复冻融。为了最大程度地回收产品,在融化后和取下盖子之前,将原始样品瓶进行离心。

Legal Information

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

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存储类别

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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Gerti Beliu et al.
Communications biology, 2, 261-261 (2019-07-26)
Genetic code expansion (GCE) technology allows the specific incorporation of functionalized noncanonical amino acids (ncAAs) into proteins. Here, we investigated the Diels-Alder reaction between trans-cyclooct-2-ene (TCO)-modified ncAAs, and 22 known and novel 1,2,4,5-tetrazine-dye conjugates spanning the entire visible wavelength range.
Evidence for a role of glutamate as an efferent transmitter in taste buds.
Vandenbeuch A, Tizzano M, Anderson CB, Stone LM, Goldberg D, Kinnamon SC
BMC Neuroscience null
Mapping the Ligand Binding Sites of Kainate Receptors: Molecular Determinants of Subunit-Selective Binding of the Antagonist [3H]UBP310.
Atlason PT, Scholefield CL, Eaves RJ, Mayo-Martin MB, Jane DE, Molnar E
Molecular Pharmacology null
Qiu-Ju Zhu et al.
FEBS letters, 586(9), 1259-1264 (2012-04-10)
Protein SUMOylation has been implicated in the pathogenesis of ischemic stroke. However, the underlying mechanisms remain unclear. Here, we found that global brain ischemia evokes a sustained elevation of GluK2 SUMOylation in the rat hippocampal CA1 region. Over-expression of wild-type
James A Daniel et al.
eLife, 6 (2017-06-10)
SUMO1-conjugation of proteins at neuronal synapses is considered to be a major post-translational regulatory process in nerve cell and synapse function, but the published evidence for SUMO1-conjugation at synapses is contradictory. We employed multiple genetic mouse models for stringently controlled

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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