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• W2056575260 abstract "Conantokins are naturally-occurring small peptide antagonists of ion flow through NMDA/glycine activated-N-methyl-d-aspartate receptor (NMDAR) ion channels. One member of the conantokin family, conantokin (con)-G, a 17-residue peptide, is selective for NMDARs containing the N-methyl-d-aspartate receptor subunit 2 B (NR2B), whereas the homologous peptides, con-T and con-R, show broader selectivity for NR2 subunits. In this study, con-G, con-R, and con-T variants were chemically synthesized and employed to investigate their subunit selectivities as inhibitors of agonist-evoked ion currents in human embryonic kidney-293 (HEK-293) cells expressing various combinations of NMDAR subunits that contain NR1a or NR1b combined with NR2A or NR2B. Using truncation and point mutants, as well as chimeric conantokins, we determined that the N-terminus of con-G contains all the determinants for NR2B selectivity. With this information, a large number of (con) variants were synthesized and used to establish minimal sequence determinants for selectivity. Tyr at position 5 broadens the NR2 selectivity, and recovery of NR2B selectivity in Tyr5 peptides was achieved by incorporating Ala or Gly at position 8. NR2B selectivity in con-R can be conferred through deletion of the Ala at position 10, thereby shifting the γ-carboxyglutamate (Gla) from position 11 to position 10, where a Gla naturally occurs in con-G and con-T. The nature of the amino acid at position 6 is also linked to subunit selectivity. Our studies suggest that the molecular determinants of conantokins that dictate NMDAR subunit selectivity are housed in specific residues of the N-termini of these peptides. Thus, it is possible to engineer desired NMDAR functional properties into conantokin-based peptides." @default.
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• W2056575260 date "2010-10-01" @default.
• W2056575260 modified "2023-10-18" @default.
• W2056575260 title "Specific determinants of conantokins that dictate their selectivity for the NR2B subunit of N-methyl-d-aspartate receptors" @default.
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• W2056575260 doi "https://doi.org/10.1016/j.neuroscience.2010.07.056" @default.
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