Selective CXCR4 antagonism by Tat: implications for in vivo expansion of coreceptor use by HIV-1 - Wikidata - wikimedia - TriplyDB

Selective CXCR4 antagonism by Tat: implications for in vivo expansion of coreceptor use by HIV-1

Selective CXCR4 antagonism by Tat: implications for in vivo expansion of coreceptor use by HIV-1

http://www.wikidata.org/entity/Q24673389

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Interaction of human dipeptidyl peptidase IV and human immunodeficiency virus type-1 transcription transactivator in Sf9 cells The C Terminus of HIV-1 Tat Modulates the Extent of CD178-mediated Apoptosis of T Cells The Glutamine-rich Region of the HIV-1 Tat Protein Is Involved in T-cell Apoptosis HIV-1 Tat, apoptosis and the mitochondria: a tubulin link?HIV-1 Tat enters T cells using coated pits before translocating from acidified endosomes and eliciting biological responses Gene expression profile of HIV-1 Tat expressing cells: a close interplay between proliferative and differentiation signals Proliferative activity of extracellular HIV-1 Tat protein in human epithelial cells: expression profile of pathogenetically relevant genes The cross-talk of HIV-1 Tat and methamphetamine in HIV-associated neurocognitive disorders Proteomics, biomarkers, and HIV-1: A current perspective Roles and functions of HIV-1 Tat protein in the CNS: an overview Cortical consequences of HIV-1 Tat exposure in rats are enhanced by chronic cocaine HIV-1 Tat Activates Neuronal Ryanodine Receptors with Rapid Induction of the Unfolded Protein Response and Mitochondrial Hyperpolarization Homonuclear (1)H-NMR assignment and structural characterization of human immunodeficiency virus type 1 Tat Mal protein The Startling Properties of Fibroblast Growth Factor 2: How to Exit Mammalian Cells without a Signal Peptide at Hand Tat acetyl-acceptor lysines are important for human immunodeficiency virus type-1 replication JM4 is a four-transmembrane protein binding to the CCR5 receptor Anxiety-like behavior of mice produced by conditional central expression of the HIV-1 regulatory protein, Tat.HIV-1 Tat protein suppresses cholangiocyte toll-like receptor 4 expression and defense against Cryptosporidium parvum.Human immunodeficiency virus-1 Tat activates calpain proteases via the ryanodine receptor to enhance surface dopamine transporter levels and increase transporter-specific uptake and Vmax.HIV-1 Tat-induced changes in synaptically-driven network activity adapt during prolonged exposure.HIV-1 Tat-induced platelet activation and release of CD154 contribute to HIV-1-associated autoimmune thrombocytopenia HIV-1 clade B Tat, but not clade C Tat, increases X4 HIV-1 entry into resting but not activated CD4+ T cells.Repeated cocaine treatment enhances HIV-1 Tat-induced cortical excitability via over-activation of L-type calcium channels.Similarity in viral and host promoters couples viral reactivation with host cell migration HIV-1 inhibits autophagy in bystander macrophage/monocytic cells through Src-Akt and STAT3.Nuclear factor-kappa B family member RelB inhibits human immunodeficiency virus-1 Tat-induced tumor necrosis factor-alpha production.Time-Dependent, HIV-Tat-Induced Perturbation of Human Neurons In Vitro: Towards a Model for the Molecular Pathology of HIV-Associated Neurocognitive Disorders Mechanism of HIV-1-TAT induction of interleukin-1beta from human monocytes: Involvement of the phospholipase C/protein kinase C signaling cascade.High-performance capillary electrophoresis for determining HIV-1 Tat protein in neurons.Genetic variation and HIV-associated neurologic disease.Ibudilast, a pharmacologic phosphodiesterase inhibitor, prevents human immunodeficiency virus-1 Tat-mediated activation of microglial cells Modifications in host cell cytoskeleton structure and function mediated by intracellular HIV-1 Tat protein are greatly dependent on the second coding exon Differential induction of interleukin-10 in monocytes by HIV-1 clade B and clade C Tat proteins.A cell-penetrating antibody fragment against HIV-1 Rev has high antiviral activity: characterization of the paratope Viral exploitation and subversion of the immune system through chemokine mimicry.The basic domain of HIV-tat transactivating protein is essential for its targeting to lipid rafts and regulating fibroblast growth factor-2 signaling in podocytes isolated from children with HIV-1-associated nephropathy.Direct effects of HIV-1 Tat on excitability and survival of primary dorsal root ganglion neurons: possible contribution to HIV-1-associated pain.Tat 101-mediated enhancement of brain pericyte migration involves platelet-derived growth factor subunit B homodimer: implications for human immunodeficiency virus-associated neurocognitive disorders.Intact lipid rafts regulate HIV-1 Tat protein-induced activation of the Rho signaling and upregulation of P-glycoprotein in brain endothelial cells The ins and outs of HIV-1 Tat.

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Selective CXCR4 antagonism by Tat: implications for in vivo expansion of coreceptor use by HIV-1

http://www.wikidata.org/entity/Q24673389

description

2000 nî lūn-bûn

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2000 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2000 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2000年の論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年论文

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P2860

Genotypic and phenotypic characterization of HIV-1 patients with primary infection

HIV-1 Entry Cofactor: Functional cDNA Cloning of a Seven-Transmembrane, G Protein-Coupled Receptor

Identification of a major co-receptor for primary isolates of HIV-1

A new classification for HIV-1

Inhibition of CXCR4-dependent HIV-1 infection by extracellular HIV-1 Tat

Cloning and functional expression of CC CKR5, a human monocyte CC chemokine receptor selective for MIP-1(alpha), MIP-1(beta), and RANTES

Identification of CCR8: a human monocyte and thymus receptor for the CC chemokine I-309

A dual-tropic primary HIV-1 isolate that uses fusin and the beta-chemokine receptors CKR-5, CKR-3, and CKR-2b as fusion cofactors

Epithelin/granulin growth factors: extracellular cofactors for HIV-1 and HIV-2 Tat proteins

Identification of RANTES, MIP-1 alpha, and MIP-1 beta as the major HIV-suppressive factors produced by CD8+ T cells

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