biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
species reactivity
human
technique(s)
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 accession no.
shipped in
dry ice
storage temp.
−20°C
Quality Level
Gene Information
human ... GRM3(2913)
mouse ... Grm3(108069)
rat ... Grm3(24416)
Immunogen
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.
Application
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.
Biochem/physiol Actions
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.
Physical form
Solution in phosphate buffered saline, containing 0.1% sodium azide.
Disclaimer
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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存储类别
10 - Combustible liquids
wgk
nwg
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
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
Dibyadeep Datta et al.
Cerebral cortex (New York, N.Y. : 1991), 33(24), 11501-11516 (2023-10-24)
Alzheimer's disease cortical tau pathology initiates in the layer II cell clusters of entorhinal cortex, but it is not known why these specific neurons are so vulnerable. Aging macaques exhibit the same qualitative pattern of tau pathology as humans, including
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
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