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Envelope surface glycoprotein gp120
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env
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HIV-1 Env gp120 upregulates Caspase-3 in SVGA cells |
PubMed
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env
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Mutational analysis shows that HIV-1 gp120 R476K and N425R are associated with the bystander apoptosis-inducing activity of Env glycoprotein through caspase 3 |
PubMed
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env
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Treatment of astrocytes with HIV-1 gp120 induces the cleavage of CASP3 as compared with untreated cells |
PubMed
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env
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HIV-1 gp120/41 Envelope proteins form a complex with integrin alpha4beta7 and chemokine receptor CCR5 on the CD4-negative gamma-delta T cell membrane, which leads to activation of the p38-caspase pathway and induces the death of gamma-delta cells |
PubMed
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env
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HIV-1 R5-tropic Env-mediated apoptosis of bystander cells is dependent on both CCR5 expression levels and fusogenic activity of the Env glycoprotein through the mechanism of apoptosis involved caspase-3 activation and mitochondrial depolarization |
PubMed
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env
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Treatment of HIV-1 Env-pseudotyped virus-infected MDM cells with both soluble TRAIL and an agonistic anti-DR5 antibody AD5-10 induces activation of caspase-3, -8, and -9 |
PubMed
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env
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HIV-1 gp120-mediated activation of caspase 8 occurs in a p53 independent manner, while HIV-1 gp120-mediated activation of caspase 3 requires p53 |
PubMed
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env
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Siva-1 sensitizes CD4-positive T-cells to HIV-1 gp120/gp41-induced apoptosis. The Siva-1-mediated sensitization on CD4-positive T-cells shows significant activation of caspase-3, -8, and -9 |
PubMed
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env
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Inactivation of PKR has an inhibitory effect on gp120-induced caspase-3 activation |
PubMed
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env
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Gp120-mediated activation of caspase-3 is significantly reduced in cells pretreated with PDGF-B |
PubMed
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env
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The combinatorial toxicity of cocaine and gp120 is accompanied by an increase in both caspase-3 activity and expression of the proapoptotic protein Bax in HIV-associated neuropathological disorders |
PubMed
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env
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The cytolytic process that takes place between primary uninfected CD4+ T cells and HIV-1 infected or HIV-1 gp120-expressing cells requires the activity of caspases such as ICE and CPP32 |
PubMed
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env
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The interaction of cell-associated HIV-1 gp120 with CXCR4-expressing target cells triggers apoptotic processes by activating caspase-9 and -3 |
PubMed
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env
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Induction of apoptosis in cell cultures through binding of HIV-1 gp120 or gp160 to CXCR4 involves protein kinase C, basic fibroblast growth factor, caspase-3, and the pro-apoptotic molecule Bax |
PubMed
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env
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Signal transducer and activator of transcription factor 1 (STAT1) partially regulates HIV-1 gp120/HCV E2-induced caspase 3 activity |
PubMed
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Envelope surface glycoprotein gp160, precursor
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env
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HIV-1 Env from Yu-2 and primary isolates activate Caspase-3 and Caspase-7 in bystander cells of co-culture assays |
PubMed
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env
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HIV-1 gp120- and gp160-induced apoptosis in cell cultures through binding to CXCR4 involves protein kinase C, basic fibroblast growth factor, caspase-3, and pro-apoptotic molecule Bax |
PubMed
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env
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HIV-1 R5-tropic Env-mediated apoptosis of bystander cells is dependent on both CCR5 expression levels and fusogenic activity of the Env glycoprotein through the mechanism of apoptosis involved caspase-3 activation and mitochondrial depolarization |
PubMed
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env
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Induction of apoptosis in cell cultures through binding of HIV-1 gp120 or gp160 to CXCR4 involves protein kinase C, basic fibroblast growth factor, caspase-3, and the pro-apoptotic molecule Bax |
PubMed
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Envelope transmembrane glycoprotein gp41
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env
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HIV-1 gp120/41 Envelope proteins form a complex with integrin alpha4beta7 and chemokine receptor CCR5 on the CD4-negative gamma-delta T cell membrane, which leads to activation of the p38-caspase pathway and induces the death of gamma-delta cells |
PubMed
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env
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HIV-1 gp41-dependent apoptosis involves caspase-3-dependent mitochondrial depolarization and reactive oxygen species production; HIV-1 gp41-induced mitochondrial depolarization is inhibited by the protease inhibitor nelfinavir |
PubMed
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env
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HIV-1 R5-tropic Env-mediated apoptosis of bystander cells is dependent on both CCR5 expression levels and fusogenic activity of the Env glycoprotein through the mechanism of apoptosis involved caspase-3 activation and mitochondrial depolarization |
PubMed
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env
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Siva-1 sensitizes CD4-positive T-cells to HIV-1 gp120/gp41-induced apoptosis. The Siva-1-mediated sensitization on CD4-positive T-cells shows significant activation of caspase-3, -8, and -9 |
PubMed
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env
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A point mutation (V38E) in the gp41 region of HIV-1 abolishes HIV-1-mediated apoptosis by CASP3 and minimizes CD4 loss in humanized mice without altering viral replication |
PubMed
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Nef
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nef
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Stable expression of HIV-1 Nef in CEM T cells activates caspase-3 and enhances apoptosis through mechanisms unrelated to Fas |
PubMed
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nef
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Stable expression of HIV-1 Nef in Jurkat T cells confers resistance to Fas-mediated apoptosis through inactivation of caspase-3 and caspase-8 |
PubMed
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nef
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Microarray and Western blot analyses have shown HIV-1 Nef-induced apoptosis in human brain micro vascular endothelial cells requires the involvement of caspase-3 and caspase-9 |
PubMed
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Pr55(Gag)
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gag
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Monocyte-derived macrophages selectively capture and engulf HIV-1-infected CD4+ T cells as HIV-1 Gag interacts with CD3 and Caspase 3 markers, leading to efficient macrophage infection |
PubMed
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Tat
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tat
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HIV-1 clade B and C Tat induce cleavage of both PARP and CASP3 in primary glia |
PubMed
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tat
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CB1 and CB2 endocannabinoid receptors are involved in HIV-1 Tat-induced cleavage of PARP1 and CASP3 in retinal cells |
PubMed
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tat
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FasL-induced activation of caspase-3 and -8 proteins is inhibited in HIV-1 Tat101-expressing Jurkat cells |
PubMed
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tat
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HIV-1 Tat induces apoptosis through activation of caspase-3 |
PubMed
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tat
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The levels of caspase-3 protein are reduced after Caco-2 cells exposure to HIV-1 Tat compared with control |
PubMed
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tat
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PDGF-BB prevents caspase-3 activation induced by HIV-1 Tat and morphine in neuroblastoma cells |
PubMed
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tat
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Tat-triggered PKCdelta and PKCtheta activation results in the downstream signaling through the apoptosis pathways mediated by both ERK1/2 and caspase-3 |
PubMed
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tat
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Co-administration of morphine and HIV-1 Tat significantly increases the percentage of neurons expressing active caspase-3 |
PubMed
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tat
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HIV-1 Tat-induced apoptosis through increased expression of anti-apoptotic protein Bcl-2, proapoptotic protein Bax and activation of caspases CASP3 and CASP9 is inhibited by estrogen receptor beta (ER)-mediated estrogen treatment |
PubMed
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tat
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A p53 fusion protein with the HIV-1 Tat basic domain at its N terminus activates the expression of p21and downregulates the levels of caspase-3 and Bcl-2 |
PubMed
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Vpr
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vpr
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Visualization of HIV-1 Vpr-induced cell cycle arrest in G2 phase and apoptosis in HeLa/Fucci2 cells is associated with caspase-3 activation |
PubMed
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vpr
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Through activation of the caspase 9 pathway, HIV-1 Vpr also activates caspase 3 |
PubMed
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vpr
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Induction of G2 cell cycle arrest by Vpr is upregulated under caspase 3-inhibition and induction of apoptosis by Vpr is downregulated by caspase 3-inhibition |
PubMed
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vpr
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Inhibition of caspase 3 by compound Z-DEVD-fmk causes accumulation of HIV-1 Vpr at the nuclear envelope. VprL23F and VprP35A mutants abrogate the sensitivity to caspase 3-inhibition |
PubMed
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vpr
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HIV-1 Vpr increases the activity of caspase-3 and caspase-9, but not of caspase-8 in human HeLa cells; Vpr-induced apoptosis can be inhibited by inhibitors of caspase-3 and caspase-9, but not by inhibitors of caspase-8 |
PubMed
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vpr
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HIV-1 Vpr-induced apoptosis results in caspase 3 cleavage |
PubMed
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vpr
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HIV-1 Vpr segments with mutation at the positions 70, 85, 86, or 94 show lower apoptosis-inducing capabilities by the attenuation of Caspase-3 activity |
PubMed
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vpr
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Virion-associated Vpr activates caspase 3/7, 8, and 9 in Fas-mediated apoptosis in Jurkat T cells and human activated PBMCs |
PubMed
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vpr
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Virion-associated Vpr triggers apoptosis through caspases 3/7 and 9 in human T cells independently of other HIV de novo-expressed proteins and also activates caspase 8, the initiator caspase of the death receptor pathway |
PubMed
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vpr
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HIV-1 Vpr-induced apoptosis through caspase activation and Smac release from mitochondria is dependent on G2 cell cycle arrest , but is lost in cells synchronized in G1/S |
PubMed
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vpr
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Overproduction of EEF2 blocks HIV-1 Vpr-induced cell death both in fission yeast and human cells, suppresses caspase 9 and caspase 3-mediated apoptosis induced by Vpr, and reduces cytochrome c release induced by Vpr |
PubMed
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Vpu
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vpu
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Caspase-8 and caspase-3 activity are required for HIV-1 Vpu-induced cleavage of IRF3 and HIV-1 infection also induces caspase-mediated IRF3 cleavage |
PubMed
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vpu
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Levels of active caspase-3 are elevated in T cells as a result of HIV-1 Vpu-mediated inhibition of NF-kappa B activation |
PubMed
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retropepsin
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gag-pol
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HIV-1 PR cleaves CASP3 to result in three processed products, Myr-lyn signal peptide, p17 and p12 proteins |
PubMed
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gag-pol
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HIV-1 protease directly cleaves and activates procaspase 8 in T cells which is associated with cleavage of BID, mitochondrial release of cytochrome c, activation of the downstream caspases 9 and 3, and cleavage of DFF and PARP |
PubMed
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