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Envelope surface glycoprotein gp120
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env
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HIV-1 gp120-induced dephosphorylation of KV2.1 is dependent on NMDA receptor-mediated activation of protein phosphatase 2B or calcineurin |
PubMed
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env
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HIV-1 gp120 activates forward trafficking and surface clustering of NMDA receptors in membrane microdomains by a PKA-dependent phosphorylation of the NR1 C-terminal Ser897, followed by a PKC-dependent phosphorylation of Ser896 |
PubMed
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env
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HIV-1 gp120-induced synapse loss requires sequential activation of CXCR4, IL-1beta receptor, and NMDA receptor |
PubMed
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env
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HIV-1 gp120 activates NMDA receptor directly and phosphorylates JNK through a gp120-mediated apoptotic pathway in human neuroblastoma cells |
PubMed
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env
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HIV-1 clade B gp120 significantly downregulates NMDA receptor gene and protein expression and levels of glutamine compared to clade C gp120 |
PubMed
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env
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HIV-1 gp120-mediated human cell death involves the NMDA receptor complex; antagonists of the NMDA receptor reverse the gp120-mediated effects |
PubMed
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env
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HIV-1 gp120 causes an activation of phospholipase A2, resulting in the increased release of arachidonic acid, which may sensitize the NMDA receptor |
PubMed
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env
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HIV-1 gp120 binds to cells expressing epsilon1/zeta1 or epsilon2/zeta1 combined NMDA receptor subunits, but not to cells expressing a single epsilon1, epsilon2, or zeta1 NMDA receptor subunit |
PubMed
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Tat
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tat
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Ca(2+) influx through the NMDA receptor is necessary for HIV-1 Tat-induced synapse loss |
PubMed
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tat
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HIV-1 Tat increases in inhibitory synapse number in neurons are dependent on LRP binding and GluN2A-containing NMDAR activation but not PSD95 ubiquitination |
PubMed
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tat
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HIV-1 Tat upregulates the expression of NMDARs for the apoptosis of retinal pigmen epithelium (RPE) cells. Silencing of NMDARs by siRNA abolishes Tat-induced RPE apoptosis |
PubMed
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tat
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HIV-1 Tat-induced activation of spermine oxidase (SMO) activity involves NMDAR stimulation in human neuroblastoma |
PubMed
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tat
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HIV-1 Tat and methamphetamine inhibit the normal conjunction of signaling between D1 and NMDA receptors, resulting in neural dysfunction and death |
PubMed
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tat
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HIV-1 Tat interacts with NMDA receptors in primary neuronal-glial cultures and in hippocampal slice cultures |
PubMed
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tat
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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 |
PubMed
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tat
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Tat treatment causes activation of neuronal nitric oxide synthase (nNOS) through association with NMDA receptors |
PubMed
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tat
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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 |
PubMed
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tat
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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 |
PubMed
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tat
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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 |
PubMed
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tat
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HIV-1 Tat induces apoptosis of neurons and neurotoxicity through the activation of both NMDA and non-NMDA receptors |
PubMed
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