|1.||Zhang, Min: 4 articles (01/2015 - 12/2011)|
|2.||Li, Wen-Bin: 3 articles (01/2015 - 12/2011)|
|3.||Hu, Yu-Yan: 3 articles (01/2015 - 12/2011)|
|4.||Gong, Jian-Xue: 2 articles (03/2012 - 12/2011)|
|5.||Gong, Shu-Juan: 2 articles (03/2012 - 12/2011)|
|6.||Xu, Jing: 1 article (01/2015)|
|7.||Wang, Dan: 1 article (01/2015)|
|8.||Li, Li: 1 article (01/2015)|
|9.||Gong, Shujuan: 1 article (06/2014)|
|10.||Wang, Jianmin: 1 article (06/2014)|
|1.||Retinoblastoma (Glioblastoma, Retinal)
03/01/1998 - "Our study demonstrates that Y-79 human retinoblastoma cells express a single Na+-dependent glutamate uptake system with a Km of 1.7 +/- 0.42 microM that is inhibited by dihydrokainate and DL-threo-beta-hydroxyaspartate (IC50 = 0.29 +/- 0.17 microM and 2.0 +/- 0.43 microM, respectively). "
06/01/2014 - "Furthermore, pre-administration of dihydrokainate, an inhibitor of GLT-1, prevented the protective effect of CIP on ischemia-induced CA1 cell death. "
01/01/2007 - "The injection of GLT-1 inhibitor (dihydrokainate) at 30 minutes before ischemia ameliorated the effect of CTX pretreatment. "
12/01/2000 - "Infusion of the GLT-1 selective nontransportable inhibitor, dihydrokainate (DHK; 1 mM) also significantly attenuated the ischemia-induced increases in both EAAs (1285 +/- 508 and 1366 +/- 741% of the preischemic levels, respectively). "
01/01/2015 - "Inhibition of GLT-1 by antisense oligodeoxynucleotides or dihydrokainate significantly inhibited the Cef-induced up-regulation in GLT-1 uptake and the neuroprotective effect against global ischemia. "
05/01/2004 - "Vehicle, dihydrokainate (DHK, 1 mmol/L), a GLT-1 inhibitor, or tamoxifen (50 micromol/L), a VRAC inhibitor, were administered continuously via the dialysis probes starting one hour prior to ischemia. "
03/01/2012 - "To explore whether GLT-1 plays a role in the acquisition of brain ischemic tolerance induced by intermittent hypobaric hypoxia (IH) preconditioning (mimicking 5,000 m high-altitude, 6 h per day, once daily for 28 days), immunohistochemistry and western blot were used to observe the changes in the expression of GLT-1 protein in hippocampal CA1 subfield during the induction of brain ischemic tolerance by IH preconditioning, and the effect of dihydrokainate (DHK), an inhibitor of GLT-1, on the acquisition of brain ischemic tolerance in rats. "
06/26/1998 - "The glutamate transport inhibitor, dihydrokainate, depressed anoxia-evoked glutamate and aspartate release. "
07/15/1999 - "Inhibition of Na(+)-dependent glutamate transport with dihydrokainate or l-trans-pyrrolidine-2,4-dicarboxylic acid (1 mm each) protected against anoxia (65-75 vs 25%) and trauma (70 vs 35%). "
04/18/1994 - "The increase in LDH release produced by hypoxia/hypoglycemia was prevented by N-methyl-D-aspartate (NMDA) antagonists, but not by three classes of drugs thought to modulate glutamate release: Ca2+ channel antagonists (nimodipine, omega-conotoxin GVIA, omega-agatoxin-IVA), KATP channel activators (cromakalim, diazoxide), and glutamate transport inhibitors (dihydrokainate, DL-threo-beta-hydroxyaspartate)."
|5.||Ganglion Cysts (Ganglion)
|1.||Glutamic Acid (Glutamate)
|2.||Amino Acid Transport System X-AG (Glutamate Transporter)
|5.||Small Interfering RNA (siRNA)
|6.||D-Aspartic Acid (D Aspartate)
|10.||Metabotropic Glutamate Receptors (Metabotropic Glutamate Receptor)