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Envelope surface glycoprotein gp120
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env
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Cells treated with monoclonal antibodies to ICAM-1 and LFA-1 adhesion molecules show an impaired release of IFN after HIV-1 gp120 stimulation, suggesting a crucial role of cell-to-cell interactions in the process leading to IFN production |
PubMed
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env
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The interaction of CD4+ T cells with HIV-1 gp120 on bilayers triggers LFA-1 activation and the LFA-1-ICAM-1 interaction rearrangement |
PubMed
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env
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HIV-1 gp120-mediated ICAM-1 expression has functional significance, as it enhances the ability of monocytic cells to bind to gp120-stimulated human astrocytes in an ICAM-1/beta 2 integrin-dependent fashion |
PubMed
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env
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HIV-1 gp120-presenting surfaces arrest the migration of primary activated CD4 T cells that occurs spontaneously in the presence of ICAM-1 and induces the formation of a virological synapse |
PubMed
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env
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Infectivity of an HIV-1 Matrix mutant that carries a suboptimal amount of HIV-1 gp120/41 is restored to a certain degree by the presence of ICAM-1 when infection is performed in cells expressing an activated form of its natural counter-ligand, LFA-1 |
PubMed
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env
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HIV-1 gp120 enhances the expression of ICAM-1 in primary human astrocytes, glioma, and endothelial cells |
PubMed
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env
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Lck phosphorylates CD3zeta and the TCR-CD3 complex is recruited to a virological synapse (VS) when cells interact with gp120+ICAM-1 bilayers, creating an F-actin-depleted zone |
PubMed
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env
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Lck is recuited to a virological synapse (VS) interface and is highly colocalized with gp120 when cells interact with gp120+ICAM-1 bilayers, leading to activation of ZAP70, LAT, SLP76, and PLCgamma |
PubMed
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env
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HIV gp120 and TNF-alpha synergistically reduce endothelial nitric oxide synthase (eNOS) expression and cause endothelial dysfunction via ICAM-1 |
PubMed
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env
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Treatment of cells with IFN reduces HIV-1 gp120 incorporation, as well as HIV-1 envelope-mediated incorporation of ICAM-1, into virions resulting in viruses that exhibit a significantly decreased ability to become bound to CD4+ target cells |
PubMed
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env
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HIV-1 gp120 activates human brain micro vascular endothelial cells (HBMEC) via CD4 in upregulating ICAM-1 and VCAM-1 expression, IL-6 secretion and increased monocyte transmigration across monolayers |
PubMed
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Envelope surface glycoprotein gp160, precursor
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env
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Antibodies against cell surface molecules LFA-1, ICAM-1, HLA-DR, and CD28 inhibit the HIV-1 gp160-induced B cell differentiation response; gp160 also induces IL-6R and CD23 molecule expression on B cells |
PubMed
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env
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ICAM-1 promotes HIV-1 gp160-mediated syncytium formation, and the ICAM-1 contrareceptor LFA-1 attenuates the syncytium-inhibiting activity of virus-neutralizing monoclonal antibodies and soluble CD4 |
PubMed
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Envelope transmembrane glycoprotein gp41
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env
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HIV-1 gp41 ectodomain fragment (amino acids 550-639) upregulates ICAM-1 on the human brain micro vascular endothelial cells (HBMECs) and elicits membrane ruffling on the surface of HBMECs |
PubMed
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env
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HIV-1 gp41 selectively enhances MHC class I, ICAM-1, IFN-alpha, IFN-beta, and IFN-omega expression in H9 cells |
PubMed
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Nef
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nef
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Microvesicles, which contaminate purified HIV-1 inocula due to similar size and density, contain viral protein Nef and cellular proteins HSP90alpha and HSP90beta that are capable of potent stimulation of dendritic cells maturation and ICAM-1 expression |
PubMed
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nef
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Expression of HIV-1 Nef in macrophages induces the release of sICAM, which upregulates the expression of co-stimulatory receptors on B lymphocytes |
PubMed
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nef
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HIV-1 Nef increases the production of exosomes, which form at the plasma membrane and co-localizes with plasma membrane-associated proteins ICAM1, CD81, and Lck in Jurkat |
PubMed
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nef
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HIV-1 Nef upregulates ICAM-1 expression on endothelial cells via Erk /Mapk signaling pathway |
PubMed
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nef
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Monoclonal antibodies to the cell surface molecule intracellular adhesion molecule (ICAM)-1 inhibit the Nef-induced B-cell differentiation response, suggesting an interaction between Nef and ICAM-1 |
PubMed
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Pr55(Gag)
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gag
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The C-terminal region (amino acids 44-132) of MA is required for ICAM-1 incorporation into HIV-1 Gag virus-like particles |
PubMed
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gag
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Acquisition of host ICAM-1 by HIV-1 occurs through an interaction between the cytoplasmic tail (residues 503-523) of ICAM-1 and HIV-1 Gag |
PubMed
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gag
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HIV-1 Gag virus-like particle-induced monocyte activation is shown by upregulation of molecules involved in antigen presentation (MHC II, CD80, CD86) and cell adhesion (CD54) |
PubMed
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gag
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ICAM-1 co-localizes with the Matrix protein of HIV-1 Gag at sites of cell-to-cell membrane contact and is incorporated into virus particles |
PubMed
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Tat
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tat
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HIV-1 Tat upregulates ICAM1 protein expression in hCMEC/D3 cells |
PubMed
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tat
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HIV-1 Tat upregulates ICAM1 mRNA and protein expression in CRT-MG human astroglioma cells |
PubMed
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tat
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HIV-1 Tat upregulates the expression of ICAM-1 in endothelial cells and astrocytes, an effect that is in part regulated by NF-kappa B and may be associated with AIDS-related Kaposi's sarcoma |
PubMed
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tat
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Microarray analysis indicates HIV-1 Tat-induced upregulation of intercellular adhesion molecule 1 (ICAM1; CD54) in primary human brain microvascular endothelial cells |
PubMed
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tat
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HIV-1 Tat-mediated upregulation of ICAM-1 expression involves reduction of miR-221/-222 expression |
PubMed
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tat
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Inhibition of human telomerase reverse transcriptase (hTERT) results in the upregulation of HIV-1 Tat-induced overexpression of intercellular adhesion molecule-1 (ICAM1) via the nuclear factor-kappaB-regulated mechanism |
PubMed
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tat
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Cell-permeable SOD inhibits the activation of MAP kinases including ERK, JNK and p38 and the upregulation of ICAM-1 and VCAM-1 by HIV-1 Tat |
PubMed
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tat
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HIV-1 Tat-induced up-regulation of VCAM-1/ICAM-1 is blocked by NADPH oxidase inhibitor |
PubMed
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tat
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Treatment of monocytes with HIV-1 Tat increases their adhesion to endothelial monolayers, an effect that is inhibited by anti-ICAM-1 Abs, suggesting an interaction between Tat and ICAM-1 |
PubMed
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Vpu
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vpu
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The expression of cellular surface ICAM-1 protein increases in cells infected with vpu-deficient HIV-1 compared to cells infected with the wild-type virus, indicating that HIV-1 Vpu downregulates ICAM-1 protein expression |
PubMed
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capsid
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gag
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ICAM-1 is weakly incorporated into HIV-1 virions when HIV-1 CA and RT (p51/p65) are concomitantly detected in Western blot |
PubMed
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gag
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Depletion of the ICAM1 expression upregulates HIV-1 CA A92E mutant infectivity in CsA-untreated HeLa cells and downregulates its infectivity in CsA-treated HeLa cells |
PubMed
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matrix
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gag
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The acidic amino acids in the MA 102-114 domain and the basic amino acids in the ICAM-1 505-513 domain are required for interaction between MA and ICAM-1, leading to ICAM-1 incorporation into virus-like particles |
PubMed
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gag
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The C-terminal region (amino acids 44-132) of MA is required for ICAM-1 incorporation into HIV-1 Gag virus-like particles |
PubMed
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gag
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Treatment of human PBMCs with HIV-1 MA upregulates the expression of MCP-1, ICAM-1, CD40, CD86 and CD36 and downregulates the expression of nuclear receptors FXR and PPARgamma |
PubMed
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gag
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ICAM-1 co-localizes with HIV-1 Matrix at sites of cell-to-cell membrane contact and is incorporated into virus particles |
PubMed
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reverse transcriptase
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gag-pol
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ICAM-1 is weakly incorporated into HIV-1 virions when HIV-1 CA and RT (p51/p65) are concomitantly detected in Western blot |
PubMed
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reverse transcriptase p51 subunit
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gag-pol
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ICAM-1 is weakly incorporated into HIV-1 virions when HIV-1 CA and RT (p51/p65) are concomitantly detected in Western blot |
PubMed
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