Raditsch M, Ruppersberg J P, Kuner T, Günther W, Schoepfer R, Seeburg P H, Jahn W, Witzemann V
Abteilung Zellphysiologie, Max-Planck-Institut für medizinische Forschung, Heidelberg, Germany.
FEBS Lett. 1993 Jun 7;324(1):63-6. doi: 10.1016/0014-5793(93)81533-6.
Cloned NMDA receptor channels of the NR1-NR2A, NR1-NR2B and NR1-NR2C type show differences in argiotoxin636 block. Mutations of an asparagine residue located at a homologous position in the TM2 region of all NMDA receptor subunits, which corresponds to the Q/R site of the AMPA receptors, alters the argiotoxin636-induced block. The results suggest that the toxin interacts at this amino acid position with the putative pore forming TM2 region of the NMDA receptor subunits. Sequence differences in the TM2 segment of NR2A and NR2C subunits are not responsible for the subtype-specific sensitivity to argiotoxin636 as revealed by site-directed mutagenesis.
克隆的NR1-NR2A、NR1-NR2B和NR1-NR2C型NMDA受体通道在银环蛇毒素636阻断方面存在差异。位于所有NMDA受体亚基TM2区域同源位置的一个天冬酰胺残基发生突变，该位置对应于AMPA受体的Q/R位点，会改变银环蛇毒素636诱导的阻断作用。结果表明，毒素在这个氨基酸位置与NMDA受体亚基假定的孔形成TM2区域相互作用。定点诱变显示，NR2A和NR2C亚基TM2片段的序列差异并非造成对银环蛇毒素636亚型特异性敏感性的原因。
