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PredicateObject
rdf:type
entrezgene:pubmed
entrezgene:interactant
entrezgene:geneRifText
Ca(2+) influx through the NMDA receptor is necessary for HIV-1 Tat-induced synapse loss, HIV-1 Tat and methamphetamine inhibit the normal conjunction of signaling between D1 and NMDA receptors, resulting in neural dysfunction and death, HIV-1 Tat induces apoptosis of neurons and neurotoxicity through the activation of both NMDA and non-NMDA receptors, HIV-1 Tat interacts with NMDA receptors in primary neuronal-glial cultures and in hippocampal slice cultures, HIV-1 Tat treatment induces the formation of complexes involving the low-density lipoprotein receptor-related protein (LRP), postsynaptic density protein-95 (PSD-95), and N-methyl-d-aspartic acid (NMDA) receptors at the neuron surface, HIV-1 Tat treatment of human neurons results in tyrosine (Y) phosphorylation at position 1325 of the NMDAR subunit 2A (NR2A) in a src kinase-dependent manner, HIV-1 Tat treatment of primary differentiated human neurons induces extensive apoptosis through increased amounts of NMDAR2A expression, but only low levels of apoptosis in primary immature human neurons result from low or minimal expression of NMDAR2A, HIV-1 Tat-induced NMDA receptor activation is clade dependent. The Cys 30-Cys 31 motif in Tat is critical for the NMDA receptor activation, Tat treatment causes activation of neuronal nitric oxide synthase (nNOS) through association with NMDA receptors
entrezgene:keyphrase
inhibits, interacts with, induces phosphorylation of, upregulates, associates with, activates, induces complex with