(Q30009092)

21 May 2017

G3BP1 restricts HIV-1 replication in macrophages and T-cells by sequestering viral RNA. (English)

1 reference

21 May 2017

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6

Siamon Gordon

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Teunis B H Geijtenbeek

7

object named as

Teunis B H Geijtenbeek

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21 May 2017

8

Neeltje A Kootstra

1 reference

Maarten A van de Klundert

21 May 2017

5

object named as

Maarten A A van de Klundert

1 reference

21 May 2017

Viviana Cobos Jiménez

1

object named as

Viviana Cobos Jiménez

1 reference

21 May 2017

Fernando O Martinez

2

1 reference

21 May 2017

Thijs Booiman

3

1 reference

21 May 2017

Karel A van Dort

4

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21 May 2017

language of work or name

English

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publication date

29 September 2015

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21 May 2017

11

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based on heuristic

inferred from page(s)

published in

Virology

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21 May 2017

486

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21 May 2017

94-104

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CD16+ monocyte-derived macrophages activate resting T cells for HIV infection by producing CCR3 and CCR4 ligands.

21 May 2017

1 reference

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Two core promotor mutations identified in a hepatitis B virus strain associated with fulminant hepatitis result in enhanced viral replication

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G3BP1, G3BP2 and CAPRIN1 are required for translation of interferon stimulated mRNAs and are targeted by a dengue virus non-coding RNA.

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Identification of host proteins required for HIV infection through a functional genomic screen

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M1 polarization of human monocyte-derived macrophages restricts pre and postintegration steps of HIV-1 replication.

7 January 2021

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M1 and M2a polarization of human monocyte-derived macrophages inhibits HIV-1 replication by distinct mechanisms.

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Re-emergence of HIV after stopping therapy

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Persistence of HIV in gut-associated lymphoid tissue despite long-term antiretroviral therapy

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Presence of an inducible HIV-1 latent reservoir during highly active antiretroviral therapy

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Towards an HIV cure: a global scientific strategy

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Bioluminescence imaging of hepatitis B virus enhancer and promoter activities in mice

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Redefining the viral reservoirs that prevent HIV-1 eradication

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Identification of a reservoir for HIV-1 in patients on highly active antiretroviral therapy

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Human MX2 is an interferon-induced post-entry inhibitor of HIV-1 infection

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Rate of HIV-1 RNA rebound upon stopping antiretroviral therapy.

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Vpx relieves inhibition of HIV-1 infection of macrophages mediated by the SAMHD1 protein

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IFI16 senses DNA forms of the lentiviral replication cycle and controls HIV-1 replication.

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Functional differences between the long terminal repeat transcriptional promoters of human immunodeficiency virus type 1 subtypes A through G.

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Evidence that ternary complex (eIF2-GTP-tRNA(i)(Met))-deficient preinitiation complexes are core constituents of mammalian stress granules

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RNA-binding proteins TIA-1 and TIAR link the phosphorylation of eIF-2 alpha to the assembly of mammalian stress granules

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Detection of AIDS virus in macrophages in brain tissue from AIDS patients with encephalopathy

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Global analysis of host-pathogen interactions that regulate early-stage HIV-1 replication

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SAMHD1 is the dendritic- and myeloid-cell-specific HIV-1 restriction factor counteracted by Vpx

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SAMHD1 restricts the replication of human immunodeficiency virus type 1 by depleting the intracellular pool of deoxynucleoside triphosphates

7 January 2021

1 reference

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Persistence of replication-competent HIV in the central nervous system despite long-term effective highly active antiretroviral therapy

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1 reference

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MCPIP1 restricts HIV infection and is rapidly degraded in activated CD4+ T cells

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Species-specific exclusion of APOBEC3G from HIV-1 virions by Vif

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Genetic programs expressed in resting and IL-4 alternatively activated mouse and human macrophages: similarities and differences

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1 reference

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Both G3BP1 and G3BP2 contribute to stress granule formation

7 January 2021

1 reference

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Critical role of an antiviral stress granule containing RIG-I and PKR in viral detection and innate immunity

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Human G3BP1 interacts with beta-F1-ATPase mRNA and inhibits its translation.

7 January 2021

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Low-level viremia persists for at least 7 years in patients on suppressive antiretroviral therapy

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Diversion of stress granules and P-bodies during viral infection

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Increased susceptibility of differentiated mononuclear phagocytes to productive infection with human immunodeficiency virus-1 (HIV-1)

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Genome-scale loss-of-function screening with a lentiviral RNAi library

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TM4: a free, open-source system for microarray data management and analysis

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Context Dependence of Different Modules for Posttranscriptional Enhancement of Gene Expression from Retroviral Vectors

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Proliferation-dependent HIV-1 infection of monocytes occurs during differentiation into macrophages

7 January 2021

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A transient three-plasmid expression system for the production of high titer retroviral vectors

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HIV-1 Nef intersects the macrophage CD40L signalling pathway to promote resting-cell infection

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The RasGAP-associated endoribonuclease G3BP assembles stress granules

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RasGAP-associated endoribonuclease G3Bp: selective RNA degradation and phosphorylation-dependent localization

7 January 2021

1 reference

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eEF2 and Ras-GAP SH3 domain-binding protein (G3BP1) modulate stress granule assembly during HIV-1 infection

7 January 2021

1 reference

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Isolation and propagation of HIV-1 on peripheral blood mononuclear cells

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Quantitative mass spectrometry of DENV-2 RNA-interacting proteins reveals that the DEAD-box RNA helicase DDX6 binds the DB1 and DB2 3' UTR structures

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Recovery of replication-competent HIV despite prolonged suppression of plasma viremia

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Probing the mRNA processing body using protein macroarrays and "autoantigenomics".

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A genome-wide short hairpin RNA screening of jurkat T-cells for human proteins contributing to productive HIV-1 replication

7 January 2021

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Human immunodeficiency virus type 1 viral protein R (Vpr) arrests cells in the G2 phase of the cell cycle by inhibiting p34cdc2 activity

7 January 2021

1 reference

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inferred from DOI database lookup

7 January 2021

based on heuristic

A third-generation lentivirus vector with a conditional packaging system

1 reference

https://api.crossref.org/works/10.1016%2FJ.VIROL.2015.09.007

inferred from DOI database lookup

7 January 2021

based on heuristic

Identifiers

DOI

10.1016/J.VIROL.2015.09.007

1 reference

Consolidated OpenCitations Corpus – April 2017

4732769

4732769

1 reference

Consolidated OpenCitations Corpus – April 2017

Consolidated OpenCitations Corpus – April 2017

1 reference