|Reactivity||Human, Mouse, Rat|
|Calculated MW||102470 Da|
|Homology||Human, mouse, dog - identical.|
|Other Names||Glutamate receptor ionotropic, kainate 2, GluK2, Glutamate receptor 6, GluR-6, GluR6, Grik2, Glur6|
|Related products for control experiments||Control peptide antigen (supplied with the antibody free of charge).|
|Target/Specificity||Peptide CSAMVEELRMSLK, corresponding to amino acid residuesֲ 858-870 of rat Kainate Receptor GluR6 (Accession P42260). Intracellular, C-terminus.|
|Peptide Confirmation||Confirmed by mass-spectrography and amino acid analysis.|
|Format||Affinity purified antibody, lyophilized powder|
|Reconstitution||50 µl or 0.2 ml deionized water, depending on the sample size.|
|Antibody Concentration After Reconstitution||0.6 mg/ml.|
|Buffer After Reconstitution||Phosphate buffered saline (PBS), pH 7.4, 1% BSA, 0.025% NaN3.|
|Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Storage After Reconstitution||The reconstituted solution can be stored at 4ºC for up to 2 weeks. For longer periods, small aliquots should be stored at -20ºC or below. Avoid multiple freezing and thawing. The further dilutions should be made using a carrier protein such as BSA (1%). Centrifuge all antibody preparations before use (10000 × g 5 min).|
|Control Antigen Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Control Antigen Reconstitution||100 µl water.|
|Control Antigen Storage After Reconstitution||-20ºC.|
|Preadsorption Control||1 µg peptide per 1 µg antibody.|
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Provided below are standard protocols that you may find useful for product applications.
L-Glutamate, the major excitatory neurotransmitter in the central nervous system (CNS), operates through several receptors that are categorized as ionotropic (ligand-gated cation channels) or metabotropic (G-protein-coupled receptors). The ligand-gated ion channel family consists of fifteen members that have been subdivided into three families based upon their pharmacological profile: the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-preferring receptors, the N-methyl-D-aspartate (NMDA)-preferring receptors, and the kainate-preferring receptors. The kainate receptor subfamily consists of five members that have been further subdivided into two classes based upon structural homology and functional characteristics. GluR5, GluR6, and GluR7 receptor subunits share a high degree of homology and are able to form functional channels when expressed in heterologous systems. The KA-1 and KA-2 receptors are unable to form functional channels on their own, but when coexpressed with GluR5-7 receptor subunits, they form channels with high affinity for kainate.1,2 Like AMPA receptors, the functional unit of endogenous kainate receptors is believed to be a tetramer, which can be either homomeric or heteromeric. Kainate receptors GluR5 and GluR6 (but not GluR7, KA-1, or KA-2) can undergo RNA editing; as in the AMPA receptor GluR2, a glutamine (Q) residue in the channel pore is edited to encode arginine (R) in the mature protein. Substitution of Q with R modulates the properties of the channel, producing channels with reduced single channel conductance and lower permeability to Ca2+.1,2 GluR6 is expressed in the CNS in basal ganglia, cerebellum, and hipoccampus, as well as in the spinal cord. The exact physiological role of GluR6 is unclear, but a role in controlling neuronal excitability, synaptic integration, and synaptic plasticity has been proposed. Abgent is pleased to offer Anti-Kainate Receptor GluK2 antibody (#AG1260), a new highly specific antibody directed against the intracellular C-terminus domain of the rat GluK2. The antibody can be used in Western blot and immunofluorescence applications and will recognize GluR6 from rat, human and mouse origins.
References 1. Lerma, J. et al. (2001) Physiol. Rev. 81, 971. 2. Dingledine, R. et al. (1999) Pharmacol. Rev. 51, 7.
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