The ion channels activated by glutamate are typically divided into two classes. Those that are sensitive to N-methyl-D-aspartate (NMDA) are designated NMDA receptors (NMDAR). The NMDAR plays an essential role in memory, neuronal development and it has also been implicated in several disorders of the central nervous system including Alzheimer’s disease, epilepsy and ischemic neuronal cell death. Increased membrane surface expression of the NR1 subunit of the receptor has been associated with synaptic plasticity. There are a number of different splice variants of the NR1. Differential splicing of three exons in the NR1 subunit generates up to eight NR1 splice variants and 7 of these have been identified in cDNA libraries. These exons encode a 21 amino acid N-terminal domain (N1) and adjacent sequences in the C-terminus (C1 and C2). Splicing out the C2 cassette eliminates the first stop codon and produces a new reading frame that generates a new sequence of 22 amino acids (C2'). Considerable attention has been focused on the distribution and expression of these splice variants that may affect the functional properties and regulation of the NMDAR.1) Grosshans, D.R., Clayton, D.A., Coultrap, S.J., and Browning, M.D., "LTP leads to rapid surface expression on NMDA not AMPA receptors in ***** rat CA1," Nature Neurosci., 5 (2002) 27 - 33. More
NMDA NR1, Splice Variant C2’ polyclonal antibody was raised against a peptide containing the C2’ insert.
IHCWB
Rat
NMDA NR1, Splice Variant C2' Antibody
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