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HIV-1 Tat through phosphorylation of NMDA
receptors potentiates glutamate excitotoxicity. / Calcium
flux in cultured rat hippocampal neurons triggered by the
transient application of glutamate or NMDA was facilitated
by pre-exposure to Tat. / Facilitation of NMDA-triggered
calcium flux by Tat was reversed by inhibitors of tyrosine
kinase (genestein and herbimycin A) and by an inhibitor of
NMDA receptor function (zinc). Tat increased 32P
incorporation into NMDA receptor subunits NR2A and NR2B and
this effect was blocked by genestein.