Envelope surface glycoprotein gp120
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env
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HIV-1 Env (gp120) binds to CD209 (DC-SIGN), which activates NFKB1 (NF-kB), MAPK1 (ERK1/2), and MAPK14 (p38) |
PubMed
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env
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HIV-1 CN54 Env (gp120) induces phosphorylation of RELA (p65), IRF3, MAPK14 (p38), and MAPK1 (ERK1/2) through TLR4 induction in monocyte derived macrophages; anti-TLR4 antibodies could inhibit this activation |
PubMed
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env
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HIV-1 gp120 induces activation of the ERK1/2 MAPK signaling pathway in polarized oral epithelial cells |
PubMed
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env
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HIV-1 gp120 activates AKT, ERK1/2, and p38 signaling in tonsil CD4+ T cells. Soluble CD4 inhibits AKT and ERK1/2 activation, but enhances phosphorylation of p38 |
PubMed
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env
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HIV-1 gp120 induces nuclear localization of the phosphoinositide-specific phospholipase C (PI-PLC) beta 1 isozyme in MDMs, which requires activation of the MAPK ERK1/2 pathway |
PubMed
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env
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HIV-1 gp120-induced phosphatidylcholine-specific phospholipase D (PLD) activity is dependent on the activation of ERK1/2 |
PubMed
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env
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Treatment of cells with HIV-1 gp120 induces increased levels of endogenous c-fos and c-jun mRNA and proteins, an activation of both c-fos and c-jun promoters, and a very rapid stimulation of the MAPK/ERK pathway |
PubMed
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env
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NHERF1 increases ERK1/2 phosphorylation levels following HIV-1 gp120 stimulation in cells |
PubMed
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env
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HIV-1 X4-tropic gp120 upregulates alpha-SMA (ACTA2) and collagen I alpha 1 expression via the ERK1/2 pathway in a CXCR4-dependent manner in activated human hepatic stellate cells |
PubMed
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env
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Stimulation of human monocyte-derived macrophages with HIV-1 gp120 results in the CCR5-mediated activation of Lyn and the concomitant Lyn-dependent activation of the mitogen-activated protein (MAP) kinase ERK-1/2, which leads to production of TNF-alpha |
PubMed
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env
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HIV-1 gp120 induces IL-10 expression in monocyte-derived dendritic cells via a mannose C-type lectin receptor and an ERK signaling pathway |
PubMed
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env
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HIV-1 gp120 activates c-Jun N-terminal kinase (JNK) and p42 extracellular-regulated kinase (ERK) in macrophages and primary human central nervous system (CNS) cells |
PubMed
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env
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Pre-treatment of endothelial cells with fibroblast growth factor 2 (FGF2) protects cells from HIV-1 gp120 angiotoxicity; this protection is regulated by crosstalk among the ERK, PI3K-AKT and PKC signaling pathways |
PubMed
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env
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Pretreatment of CD4+ T cells with HIV-1 gp120 followed by stimulation with jacalin results in marked inhibition of phosphorylation of ERK2 as well as JNK |
PubMed
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Envelope surface glycoprotein gp160, precursor
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env
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The activation of mitogen-activated protein kinases (MAPKs, including ERK, JNK, and p38MAPK) is induced by incubation of HIV-1 gp160 with CD4+complement receptor type 2 (CR2)+ cells |
PubMed
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env
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Pre-incubation of CD4+ T lymphocytes with anti-CD4 mAb or HIV-1 gp160 inhibits the activation of c-Jun N-terminal kinases (JNK) and extracellular signal-regulated protein kinase 2 (ERK2) in response to phorbol 12-myristate 13-acetate and ionomycin |
PubMed
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Envelope transmembrane glycoprotein gp41
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env
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The HIV-1 gp41 transmembrane domain inhibits TLR2-induced activation of ERK1/2, and secretion of TNF-alpha, MCP-1, and IL-6 |
PubMed
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env
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HIV-1 gp41 is able to activate the ERK/MAPK pathway by binding to CD74 |
PubMed
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Nef
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nef
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HIV-1 Nef-induced strong activation of MAP kinases (p38/MAPK14, JNK/MAPK8, and ERK1/2) and NF-kappaB pathway (IKK alpha/beta) in M2-macrophages is mediated by TAK1 |
PubMed
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nef
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HIV-1 Nef induces phosphorylation of MAPK1 (ERK2) in M2-type macrophages |
PubMed
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nef
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HIV-1 Nef expression in a human astrocytic cell line inhibits the endothelin-1 mediated activation of ERK1 and ERK2 activity |
PubMed
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nef
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The Nef/hnRNPK/PKC-delta/Hck protein complex increases paxillin phosphorylation at Y118 and activates and secretes TACE through Erk1/2 activation |
PubMed
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nef
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HIV-1 Nef causes the FMS N-glycosylation defect and induces relocalization of the GM130 by activating the p56Hck/MEK/ERK/GRASP65 phosphorylation cascade in the Golgi |
PubMed
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nef
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HIV-1 Nef-induced relocalization of LCK increases phosphorylated ERK1/2 induction in infected and trasduced primary T cells |
PubMed
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nef
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Formation of the Nef-associated kinase complex (NAKC) is sufficient to activate LCK and ERK1/2 and causes a strong Tat-dependent increase of HIV-1 transcription in T cells |
PubMed
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nef
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The formation of Nef/LCK/PKCtheta complex activates the ERK MAPK signaling pathway |
PubMed
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nef
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HIV-1 Nef and ALK are capable of cumulatively influencing the MAP-K phosphorylation in astrocytic glioma cells |
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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A proline-rich repeat sequence [(Pxx)4] in HIV-1 Nef occurring between amino acid residues 69 to 78 binds to MAPK and significantly decreases its kinase activity in vitro |
PubMed
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nef
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HIV-1 Nef, through its PxxP and RR106 motifs, upregulates Src kinase activity and signal transducer and activator of transcription 3 (Stat3) phosphorylation, and activates the Ras-c-Raf-MAPK1,2 pathway in podocytes |
PubMed
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nef
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HIV-1 Nef induces ERK/MAPK signaling, which is essential for Nef-mediated Bcl-XL upregulation and cell survival in TF-1 macrophages cells |
PubMed
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nef
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In human and murine monocyte-macrophages, HIV-1 Nef induces both DNA binding and transcriptional activities of the activator protein-1 (AP-1) through an association with ERK1 and 2 signaling pathways |
PubMed
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nef
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HIV-1 Nef-induced Fas ligand transcription is regulated by p38 MAPK-mediated activator protein-1 (AP-1) activation |
PubMed
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nef
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HIV-1 Nef expression in primary CD4 T cells upregulates ERK, MEK, and Elk induction in a T cell receptor stimulation dependent manner, leading to enhanced viral replication and infectivity |
PubMed
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nef
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Phospho-MAPK1,2 and phospho-Stat3 staining increase in podocytes of kidneys from HIV-associated nephropathy patients, suggesting HIV-1 Nef-induced activation of these pathways is responsible for podocyte proliferation and dedifferentiation |
PubMed
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nef
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MAPK and JNK activities are activated in the presence of HIV-1 Nef after TNF-alpha treatment in human glial cells |
PubMed
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nef
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The activation of extracellular signal-regulated kinase 2 (ERK2) by endothelin-1 (ET-1) is inhibited by HIV-1 Nef in human astrocytes; a similar inhibitory action of Nef on ERK2 activation was observed after direct stimulation of G proteins |
PubMed
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Pr55(Gag)
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gag
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ERK2 phosphorylates HIV-1 CA at position Ser16 residue after the initiation of HIV-1 Gag processing by HIV-1 PR |
PubMed
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gag
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The CA region of HIV-1 Gag interacts with MAPK/ERK2 and sequentially encapsidates MAPK/ERK2 into virus particles. A domain comprising amino acids 56-110 in CA is critical for Gag interaction with MAPK/ERK2 |
PubMed
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gag
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The p6 protein of HIV-1 Gag is phosphorylated by cellular kinases with ERK1 and ERK2 being the most likely kinases involved in p6 phosphorylation |
PubMed
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gag
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Phosphorylation of the Matrix protein of HIV-1 Gag on tyrosine and serine facilitates dissociation of Matrix from the cellular membrane, thus allowing it to translocate to the nucleus and participate in HIV-1 nuclear import |
PubMed
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gag
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Recombinant MAPK phosphorylates the Matrix protein of HIV-1 Gag on serine and threonine residues, whereas immunoprecipitated MAPK predominantly phosphorylates Matrix on serine residues |
PubMed
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Rev
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rev
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MAPK has been shown to phosphorylate Rev in vitro |
PubMed
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Tat
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tat
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HIV-1 Tat protein activates RELA (p65), MAP kinases ERK1/2 and p38, and PKC-bII in a TLR4-dependent manner in human monocytes |
PubMed
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tat
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HIV-1 Tat activates PRKCQ (PKC-theta) kinase activity, which leads to RELA (NFkB), NRAS, RAF1, MAP2K1 (MEK1), MAP2K2 (MEK2), MAPK3 (ERK1), and MAPK1 (ERK2) activation, in Jurkat T cells that stably express Tat |
PubMed
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tat
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HIV-1 Tat induces phosphorylation of MAPK1 (ERK2) in CRT-MG human astroglioma cells |
PubMed
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tat
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HIV-1 Tat increases phosphorylation of ERK1/2, JNK1/2, p38, AKT1, MEK-1, and STAT-1alpha in Muller glia and brain microvascular pericytes |
PubMed
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tat
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Treatment with HIV-1 Tat induces phosphorylation of ERK1/2 and JNK in brain micro vascular endothelial cells (BMEC) and astrocytes, which mediates Tat-induced multidrug resistance-associated protein 1 (MRP1) expression |
PubMed
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tat
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Blocking HIV-1 Tat and cocaine-mediated Erk activation reverses ZO-1 downregulation in human pulmonary artery endothelial cells |
PubMed
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tat
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Treatment with HIV-1 Tat and cocaine activates Ras/Erk pathway in human pulmonary artery endothelial cells |
PubMed
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tat
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Treatment with HIV-Tat and morphine activates extracellular signal-regulated kinase-1/2 (ERK1/2), upregulates p53 and p21 levels, and downregulates cyclin D1 and Akt levels in human fetal brain-derived neural precursor cells |
PubMed
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tat
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The basic domain (49RKKRRQRRR57) of HIV-1 Tat is essential for enhancing the FGF-induced activation of ERK, Rho-A, and MLC2 and upregulates the expression of MMP-9 in human podocytes |
PubMed
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tat
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HIV-1 Tat induces activation of the ERK1/2 MAPK signaling pathway in polarized oral epithelial cells |
PubMed
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tat
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HIV-1 Tat- and oxovanadate-treated microglial cells synergistically induce release of TNF-alpha and IL-1beta proteins, which involves CD45 and ERK1/2 signaling pathways |
PubMed
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tat
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HIV-1 Tat induces ERK phosphorylation by the activation of the small GTPase Ras, but not the small GTPase Rac, in human endothelial cells |
PubMed
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tat
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Knocking down Nox2 by siRNA decreases HIV-1 Tat-induced NF-KappaB activation as well as activation of MAP kinases including ERK, JNK, and p38 |
PubMed
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tat
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HIV-1 Tat-induced upregulation of B7-H1 protein expression requires activation of the ERK/MAPK signaling pathway in human endothelial cells |
PubMed
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tat
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HIV-1 Tat and morphine-induced apoptosis in human neuroblastoma cells involves ERK1/2 and JNK activation |
PubMed
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tat
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Adhesion of endothelial cells to HIV-1 Tat triggers a signal transduction pathway, which leads to phosphorylation of VEGFR2 and pp60src and activation of ERK1/2 |
PubMed
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tat
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HIV-1 Tat-linked intracellular third loop of the endothelin-1 type B receptor markedly enhances the endothelin-1 activation of ERK in the bone morphogenetic protein-2 receptor human pulmonary artery smooth muscle cells |
PubMed
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tat
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The NADPH oxidase inhibitors DPI and apocynin abrogate HIV-1 Tat-stimulated ERK1/2 activation in human microglia-like cells |
PubMed
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tat
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HIV-1 Tat inhibits the LPS-activation of ERK1/2 but not the p38 mitogen-activated protein kinases in primary blood monocytes/macrophages |
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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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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Tat and IFN-gamma synergistically induce the expression of CXCL10, which is inhibited by MEK1/2 inhibitor and the p38 mitogen-activated protein kinase (MAPK) inhibitor |
PubMed
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tat
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Formation of the Nef-associated kinase complex (NAKC) is sufficient to activate LCK and ERK1/2 and causes a strong Tat-dependent increase of HIV-1 transcription in T cells |
PubMed
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tat
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HIV-1-Tat-mediated upregulation of platelet-derived growth factor (PDGF) B chain in astrocytes is regulated by activation of ERK1/2 and JNK MAPK signaling pathways and the downstream transcription factor early growth response 1 (Egr1) |
PubMed
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tat
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Tat activates at least three signaling pathways concurrently, including NF-kappaB, PKC, ERK1/2 and p38 MAP kinases and IKKalpha pathways, to promote production of IL-10 |
PubMed
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tat
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Sulfated polymannuroguluronate (SPMG) blocks the Tat-induced extracellular-signal regulated kinase 1/2- and c-jun amino-terminal kinase-mediated signalling pathways |
PubMed
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tat
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The binding between HIV-1 Tat and Grb2 is mediated by the proline-rich sequence (residues 1-18) of Tat and the SH3 domain (residues 160-212) of Grb2, which impairs activation of the Raf/MAPK pathway and increases the PKA/Raf inhibitory pathway |
PubMed
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tat
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HIV-1 Tat-induced MAPK (ERK, JNK, and p38) activation is required for MMP-9 expression in human astrocytes |
PubMed
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tat
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HIV-1 Tat in combination with KSHV kaposin A activates the MEK/ERK, STAT3, and PI3K/Akt signals in NIH3T3 cells |
PubMed
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tat
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Phospholipase C/protein kinase C signaling pathway-dependent phosphorylation of p44/42 and JNK MAP kinases participates partially in IL-1beta induction by TAT |
PubMed
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tat
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HIV-1 Tat alters the properties of human neural precursor cells via attenuation of the cell cycle regulatory unit cyclin D1 and the mitogen-activated protein kinase (MAPK) pathway, particularly extracellular signal-related kinase 1/2 (ERK1/2) |
PubMed
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tat
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HIV-1 Tat-induced glutamate release is mediated through p38 and p42/44 MAPK and through NADPH oxidase and the x(c)(-) cystine-glutamate antiporter (xCT) |
PubMed
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tat
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HIV-1 Tat activates ERK1 and ERK2 through the activation of MEK1 and MEK2, leading to induction of IL-8, IL-10, IP-10, iNOS, superoxide and TNF-alpha, as well as suppression of p35 activator of cdk5, activation of CREB and increased albumin permeability |
PubMed
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tat
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Expression of HIV-1 Tat in human SK-N-MC cells inhibits the NGF-signaling pathway leading to suppression of MAPK and reduction of Puralpha binding to the Egr-1 promoter |
PubMed
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tat
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HIV-1 Tat is phosphorylated by MAPK in vitro |
PubMed
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tat
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The interaction of HIV-1 Tat with KDR/VEGFR2 is implicated in the activation of ERK1 and ERK2 signaling pathways |
PubMed
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Vif
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vif
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MAPK phosphorylates HIV-1 Vif on Thr96 and Ser165 and is important in the regulation of HIV-1 infectivity by Vif |
PubMed
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Vpr
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vpr
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HIV-1 Vpr-induced caspase-8 activation causes cleavage of BID to tBID through ERK activation |
PubMed
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capsid
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gag
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ERK2 is incorporated into newly formed viral particles via its interaction with HIV-1 Gag and phosphorylates HIV-1 CA at Ser16 residue in virions. ERK2-packaging-defective virus exhibits lower infectivity than control virus |
PubMed
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integrase
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gag-pol
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Analysis of HIV-1 proviral integration sites in antiretroviral treatment patients indicates that MAPK1 gene favors HIV-1 integration for expansion and persistence of infected cells, suggesting HIV-1 IN interacts with MAPK1 |
PubMed
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matrix
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gag
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HIV-1 MA natural variant S75X-mediated proliferation of both Epstein-Barr virus (EBV)-infected primary and fully transformed B-lymphocytes requires AKT, ERK1/2, and STAT3 pathways |
PubMed
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gag
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HIV-1 p17 variant S75X shows a similar activity to p17delta36 in modulating ERK1/2 signalling pathway in Raji and human primary B cells |
PubMed
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gag
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Expression of Pokeweed antiviral protein (PAP), a plant-derived N-glycosidase, activates the ERK1/2 MAPK pathway to a limited extent, resulting in increased phosphorylation of HIV-1 MA |
PubMed
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gag
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HIV-1 p17 induces phosphorylation of ERK1/ERK2 in human endothelial cells |
PubMed
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gag
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HIV-1 p17 induces capillary-like structures in human endothelial cells by binding to CXCR1 and CXCR2, which requires activation of the Akt-dependent ERK signaling pathway |
PubMed
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gag
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HIV-1 MA increases phosphorylation and the DNA-binding activity of CREB and c-Myc through activation of the cAMP/PKA and MEK/ERK signaling pathways. Both signaling pathways are synergistically activated upon co-stimulation through the CD19 receptor |
PubMed
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gag
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Phosphorylation of HIV-1 Matrix on tyrosine and serine prior to and during virus infection facilitates dissociation of Matrix from the cellular membrane, thus allowing it to translocate to the nucleus and participate in HIV-1 nuclear import |
PubMed
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gag
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Recombinant MAPK phosphorylates HIV-1 Matrix on serine and threonine residues, whereas immunoprecipitated MAPK predominantly phosphorylates HIV-1 Matrix on serine residues |
PubMed
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p6
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gag
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HIV-1 p6-Gag is phosphorylated by cellular kinases with ERK1 and ERK2 being the most likely kinases involved in p6 phosphorylation |
PubMed
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reverse transcriptase
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gag-pol
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MEK1 in HIV-1 producer cells is able to activate virion-associated MAPK in trans, and the activated MAPK facilitates efficient disengagement of the HIV-1 reverse transcription complex from the cell membrane and subsequent nuclear translocation |
PubMed
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