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Merck
CN

G1545

Sigma-Aldrich

Anti-Glutamate Receptor 3, Metabotropic antibody produced in rabbit

affinity isolated antibody, buffered aqueous solution

别名:

Anti-mGluR3

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MDL编号:
UNSPSC代码:
12352203
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生物来源

rabbit

质量水平

偶联物

unconjugated

抗体形式

affinity isolated antibody

抗体产品类型

primary antibodies

克隆

polyclonal

表单

buffered aqueous solution

种属反应性

human

技术

immunocytochemistry: 38 μg/mL using human brain, neurons and glia
immunohistochemistry (formalin-fixed, paraffin-embedded sections): 38 μg/mL using human brain, neurons and glia
western blot: suitable

UniProt登记号

运输

dry ice

储存温度

−20°C

基因信息

human ... GRM3(2913)
mouse ... Grm3(108069)
rat ... Grm3(24416)

免疫原

synthetic peptide corresponding to the N-terminal extracellular domain of human metabotropic glutamate receptor 3, conjugated to KLH. The immunizing peptide has 100% homology with the rat and mouse gene.

应用

Anti-Glutamate Receptor 3, Metabotropic antibody produced in rabbit is suitable for:
  • western blot analysis of mouse somatosensory cortex to examine the connexin 36 (Cx36) protein expression and electrotonic coupling incidence.
  • western blot analysis of rat hypothalamus to study the Cx36 expression.
  • immunocytochemistry (formalin-fixed, paraffin-embedded sections) at a concentration of 38μg/mL using human brain, neurons and glia.

生化/生理作用

Glutamate, the excitatory neurotransmitter, is involved in fast excitatory synaptic transmission. It acts on ligand-gated receptor channels, termed NMDA, AMPA and kainate receptors. The metabotropic form consist of eight subtypes (mGluR1-8) divided into three groups (I-III). Group I binds to phospholipase C and intracellular calcium mobilization, whereas both groups II and III inhibit adenyl cyclase. The metabotropic receptors have some therapeutic potentials. Group I receptors have been implicated in post-ischemic neuronal injury, and antagonists of group I appear to have a neuroprotective effect.

外形

Solution in phosphate buffered saline, containing 0.1% sodium azide.

免责声明

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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储存分类代码

10 - Combustible liquids

WGK

nwg

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

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分析证书(COA)

Lot/Batch Number

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Lu E Jin et al.
Cerebral cortex (New York, N.Y. : 1991), 28(3), 974-987 (2017-01-22)
The newly evolved circuits in layer III of primate dorsolateral prefrontal cortex (dlPFC) generate the neural representations that subserve working memory. These circuits are weakened by increased cAMP-K+ channel signaling, and are a focus of pathology in schizophrenia, aging, and
Won-Mee Park et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 31(16), 5909-5920 (2011-04-22)
Coupling of neurons by electrical synapses (gap junctions) transiently increases in the mammalian CNS during development. We report here that the developmental increase in neuronal gap junction coupling and expression of connexin 36 (Cx36; neuronal gap junction protein) are regulated
Elizabeth Woo et al.
Frontiers in neuroanatomy, 16, 849937-849937 (2022-04-22)
Metabotropic glutamate receptors type 3 (mGlu3, encoded by GRM3) are increasingly related to cognitive functioning, including the working memory operations of the prefrontal cortex (PFC). In rhesus monkeys, mGlu3 are most commonly expressed on glia (36%), but are also very
Yongfu Wang et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 32(2), 713-725 (2012-01-13)
In the mammalian CNS, excessive release of glutamate and overactivation of glutamate receptors are responsible for the secondary (delayed) neuronal death following neuronal injury, including ischemia, traumatic brain injury (TBI), and epilepsy. The coupling of neurons by gap junctions (electrical
Dibyadeep Datta et al.
Frontiers in aging neuroscience, 13, 760270-760270 (2021-12-07)
Glutamate carboxypeptidase II (GCPII) expression in brain is increased by inflammation, and reduces NAAG (N-acetyl aspartyl glutamate) stimulation of mGluR3 signaling. Genetic insults in this signaling cascade are increasingly linked to cognitive disorders in humans, where increased GCPII and or

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