| 生物活性： |
背景说明：Tat-NR2BAA 是 Tat-NR2B9c (HY-P0117) 的对照肽 (control peptide)，没有活性。Tat-NR2BAA 的序列与 Tat-NR2B9c 相似，但在 COOH 末端 tSXV 基序中有一个双点突变，这使得它无法结合 PSD-95。Tat-NR2B9c 是一种可通透细胞膜的多肽，破坏 PSD-95/NMDAR 的结合。Tat-NR2BAA is the control peptide of Tat-NR2B9c (HY-P0117), inactive. The sequence of Tat-NR2BAA is similar to Tat-NR2B9c, but it has a double-point mutation in the COOH terminal tSXV motif, making it incapable of binding PSD-95. Tat-NR2B9c is a membrane-permeant peptide and disrupts PSD-95/NMDAR binding, correlate with uncoupling NR2B-and/or NR2A-type NMDARs from PSD-95.
In Vitro：Tat-NR2BAA (125 ng; 20 mins) does not effects interactions between PSD-95 and NR2B subunits. In contrast, coimmunoprecipitation of PSD-95 with NR2B subunits is markedly decreased in rats pretreated with the disrupting peptide Tat-NR2B9c in lumbar dorsal horn tissue.
Tat-NR2Baa (125 ng or 1.25 μg; 20 minutes before collection of lumbar dorsal horn tissue) is the control group of Tat-NR2B9c. Tat-NR2B9c produces a significant and robust reduction of postdischarge, indicating the hyperexcitability of the cell. But Tat-NR2Baa has no effects, even at a dose 100× greater than the active peptide Tat-NR2B9c (HY-P0117).
Tat-NR2Baa (1 μM; pre-treatment 1 hour) is the control group in the Co-IP assay. Tat-NR2B9c (1 μM) disrupts NR2B/PSD95 interaction, and the coupling of NR2B to PSD-95 is more sensitive than NR2A/PSD95 to disruption in hippocampal neurons.
参考文献：[1] Aarts M, Liu Y, Liu L, et al. Treatment of ischemic brain damage by perturbing NMDA receptor-PSD-95 protein interactions[J]. Science, 2002, 298(5594): 846-850.
|
扫一扫关注我们
