Endogenous factors enhance HIV infection of tissue naive CD4 T cells by stimulating high molecular mass APOBEC3G complex formation - Wikidata - awgldk - TriplyDB

Endogenous factors enhance HIV infection of tissue naive CD4 T cells by stimulating high molecular mass APOBEC3G complex formation

Endogenous factors enhance HIV infection of tissue naive CD4 T cells by stimulating high molecular mass APOBEC3G complex formation

http://www.wikidata.org/entity/Q36228592

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The dimerization domain of HIV-1 viral infectivity factor Vif is required to block virion incorporation of APOBEC3G HIV-1 Vif versus the APOBEC3 cytidine deaminases: an intracellular duel between pathogen and host restriction factors Prototype foamy virus Bet impairs the dimerization and cytosolic solubility of human APOBEC3G HIV-1 Vif, APOBEC, and intrinsic immunity WFDC1/ps20 is a novel innate immunomodulatory signature protein of human immunodeficiency virus (HIV)-permissive CD4+ CD45RO+ memory T cells that promotes infection by upregulating CD54 integrin expression and is elevated in HIV type 1 infection Dendritic Cells in HIV-1 and HCV Infection: Can They Help Win the Battle?Crystal Structure of the DNA Cytosine Deaminase APOBEC3F: The Catalytically Active and HIV-1 Vif-Binding Domain Dissecting How CD4 T Cells Are Lost During HIV Infection APOBEC3G: an intracellular centurion T cells contain an RNase-insensitive inhibitor of APOBEC3G deaminase activity.Vpr14-88-Apobec3G fusion protein is efficiently incorporated into Vif-positive HIV-1 particles and inhibits viral infection.Functions and regulation of the APOBEC family of proteins Friend or Foe: Innate Sensing of HIV in the Female Reproductive Tract.Innate and adaptive immune correlates of vaccine and adjuvant-induced control of mucosal transmission of SIV in macaques.Abortive HIV infection mediates CD4 T cell depletion and inflammation in human lymphoid tissue.Establishment of HIV-1 latency in resting CD4+ T cells depends on chemokine-induced changes in the actin cytoskeleton.HIV-1 Nef: a multifaceted modulator of T cell receptor signaling.The cellular source for APOBEC3G's incorporation into HIV-1.A unified concept of HIV latency.Active lytic infection of human primary tonsillar B cells by KSHV and its noncytolytic control by activated CD4+ T cells.Viral exploitation of host SOCS protein functions APOBEC3G: a double agent in defense The roles of APOBEC3G complexes in the incorporation of APOBEC3G into HIV-1.High-molecular-mass APOBEC3G complexes restrict Alu retrotransposition.Direct evidence that RNA inhibits APOBEC3G ssDNA cytidine deaminase activity.HIV Latency Is Established Directly and Early in Both Resting and Activated Primary CD4 T Cells.In vitro activities of candidate microbicides against cell-associated HIV A Peptide Derived from the HIV-1 gp120 Coreceptor-Binding Region Promotes Formation of PAP248-286 Amyloid Fibrils to Enhance HIV-1 Infection.Emerging complexities of APOBEC3G action on immunity and viral fitness during HIV infection and treatment.APOBEC3G/3F mediates intrinsic resistance of monocyte-derived dendritic cells to HIV-1 infection The DNA deaminase activity of human APOBEC3G is required for Ty1, MusD, and human immunodeficiency virus type 1 restriction.IFN-α and lipopolysaccharide upregulate APOBEC3 mRNA through different signaling pathways.HIV-1 Vif promotes the formation of high molecular mass APOBEC3G complexes.HIV envelope-CXCR4 signaling activates cofilin to overcome cortical actin restriction in resting CD4 T cells Interleukin-2 inhibits HIV-1 replication in some human T cell lymphotrophic virus-1-infected cell lines via the induction and incorporation of APOBEC3G into the virion.Double-stranded RNA analog poly(I:C) inhibits human immunodeficiency virus amplification in dendritic cells via type I interferon-mediated activation of APOBEC3G.Vif and Apobec3G in the innate immune response to HIV: a tale of two proteins.AID can restrict L1 retrotransposition suggesting a dual role in innate and adaptive immunity Host Factors and HIV-1 Replication: Clinical Evidence and Potential Therapeutic Approaches An HIV-1 replication pathway utilizing reverse transcription products that fail to integrate.

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P2860

Endogenous factors enhance HIV infection of tissue naive CD4 T cells by stimulating high molecular mass APOBEC3G complex formation

http://www.wikidata.org/entity/Q36228592

description

2006 nî lūn-bûn

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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2006年论文

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2006年论文

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name

Endogenous factors enhance HIV ...... ass APOBEC3G complex formation

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Endogenous factors enhance HIV ...... ass APOBEC3G complex formation

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Endogenous factors enhance HIV ...... ass APOBEC3G complex formation

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Endogenous factors enhance HIV ...... ass APOBEC3G complex formation

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Endogenous factors enhance HIV ...... ass APOBEC3G complex formation

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Journal of Experimental Medicine

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Endogenous factors enhance HIV ...... ass APOBEC3G complex formation

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Warner C Greene

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Wes Yonemoto

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P2860

HIV-1 Vif blocks the antiviral activity of APOBEC3G by impairing both its translation and intracellular stability

HIV-1 entry into quiescent primary lymphocytes: molecular analysis reveals a labile, latent viral structure

HIV does not replicate in naive CD4 T cells stimulated with CD3/CD28

Massive infection and loss of memory CD4+ T cells in multiple tissues during acute SIV infection

Population biology of HIV-1 infection: viral and CD4+ T cell demographics and dynamics in lymphatic tissues.

Preferential infection of CD4+ memory T cells by human immunodeficiency virus type 1: evidence for a role in the selective T-cell functional defects observed in infected individuals

Both memory and CD45RA+/CD62L+ naive CD4(+) T cells are infected in human immunodeficiency virus type 1-infected individuals

Resting naive CD4+ T cells are massively infected and eliminated by X4-tropic simian-human immunodeficiency viruses in macaques

HIV-1 replication is controlled at the level of T cell activation and proviral integration.

In vivo HIV-1 infection of CD45RA(+)CD4(+) T cells is established primarily by syncytium-inducing variants and correlates with the rate of CD4(+) T cell decline

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865-870

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10.1084/JEM.20051856

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4

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203

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Jason F Kreisberg

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7172740

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2118295

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