Search results for Glutamate Receptor 2 (GRIA2) Antibody
Glutamate Receptor 2 (GRIA2) Antibody, Abbexa, abx010851
Glutamate receptors are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. This gene product belongs to a family of glutamate receptors that are sensitive to alpha amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), and function as ligand-activated cation channels. These channels are assembled from 4 related subunits, Gria1-4. The subunit encoded by this gene (Gria2) is subject to RNA editing (Q/R and R/G), which is thought to render the channels impermeable to Ca (2+), and to affect the kinetic aspects of these channels in rat brain. Alternative splicing, resulting in transcript variants encoding different isoforms (flip and flop), has been noted for this gene.
Host
Mouse
Reactivity
Human
Applications
ELISA, WB, FCM
Conjugation
Unconjugated
Glutamate Receptor 2 (GRIA2) Antibody, Abbexa, abx455340
Glutamate Receptor 2 (GRIA2) Antibody is a Rabbit polyclonal antibody for the detection of Human Glutamate Receptor 2 (GRIA2).
Host
Rabbit
Reactivity
Human
Applications
ELISA, WB, IHC
Conjugation
Unconjugated
Glutamate Receptor 2 (GRIA2) Antibody, Abbexa, abx000558
GRIA2 Antibody is a Rabbit Polyclonal antibody against GRIA2. Glutamate receptors are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. This gene product belongs to a family of glutamate receptors that are sensitive to alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), and function as ligand-activated cation channels. These channels are assembled from 4 related subunits, GRIA1-4. The subunit encoded by this gene (GRIA2) is subject to RNA editing (CAG->CGG; Q->R) within the second transmembrane domain, which is thought to render the channel impermeable to Ca(2+). Human and animal studies suggest that pre-mRNA editing is essential for brain function, and defective GRIA2 RNA editing at the Q/R site may be relevant to amyotrophic lateral sclerosis (ALS) etiology. Alternative splicing, resulting in transcript variants encoding different isoforms, (including the flip and flop isoforms that vary in their signal transduction properties), has been noted for this gene.
Host
Rabbit
Reactivity
Human, Mouse, Rat
Applications
WB
Conjugation
Unconjugated
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