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Envelope surface glycoprotein gp120
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env
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HIV-1 gp120 induced-neurotoxicity involves upregulation of NR2B and downregulation of PSD-95 expressions in neuron cells |
PubMed
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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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The gene expression of GRIN2B is significantly upregulated in both clade B and clade C Tat treated SK-N-MC neuroblastoma cells |
PubMed
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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 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-induced loss of presynaptic terminals is recovered by ifenprodil, an NR2B subunit-selective NMDA receptor antagonist |
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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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 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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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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