HIV-1 Nef inhibits ASK1-dependent death signalling providing a potential mechanism for protecting the infected host cell (Q24291113)

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author name string

R Geleziunas

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W Xu

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W C Greene

Does HIV cause depletion of CD4+ T cells in vivo by the induction of apoptosis?

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language of work or name

English

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publication date

12 April 2001

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published in

Nature

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volume

410

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issue

6830

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page(s)

834-8

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cites work

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7 January 2021

Apoptosis occurs predominantly in bystander cells and not in productively infected cells of HIV- and SIV-infected lymph nodes

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Evasion of cytotoxic T lymphocyte (CTL) responses by nef-dependent induction of Fas ligand (CD95L) expression on simian immunodeficiency virus-infected cells.

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Induction of Fas ligand expression by HIV involves the interaction of Nef with the T cell receptor zeta chain

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Induction of fas ligand expression by an acutely lethal simian immunodeficiency virus, SIVsmmPBj14.

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Fas antigen stimulation induces marked apoptosis of T lymphocytes in human immunodeficiency virus-infected individuals.

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Activation of apoptosis signal-regulating kinase 1 (ASK1) by the adapter protein Daxx

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Induction of apoptosis by ASK1, a mammalian MAPKKK that activates SAPK/JNK and p38 signaling pathways

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ASK1 is essential for JNK/SAPK activation by TRAF2

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Macrophage-dependent apoptosis of CD4+ T lymphocytes from HIV-infected individuals is mediated by FasL and tumor necrosis factor

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Apoptosis of CD8+ T cells is mediated by macrophages through interaction of HIV gp120 with chemokine receptor CXCR4.

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HIV-1 upregulates Fas ligand expression in CD4+ T cells in vitro and in vivo: association with Fas-mediated apoptosis and modulation by aurintricarboxylic acid

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Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1.

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Activation of apoptosis signal-regulating kinase 1 (ASK1) by tumor necrosis factor receptor-associated factor 2 requires prior dissociation of the ASK1 inhibitor thioredoxin.

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A conserved domain and membrane targeting of Nef from HIV and SIV are required for association with a cellular serine kinase activity

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Crystal structure of the conserved core of HIV-1 Nef complexed with a Src family SH3 domain

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Nef-induced CD4 and major histocompatibility complex class I (MHC-I) down-regulation are governed by distinct determinants: N-terminal alpha helix and proline repeat of Nef selectively regulate MHC-I trafficking

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The SH3 domain-binding surface and an acidic motif in HIV-1 Nef regulate trafficking of class I MHC complexes

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A dileucine motif in HIV-1 Nef acts as an internalization signal for CD4 downregulation and binds the AP-1 clathrin adaptor

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A dileucine motif in HIV-1 Nef is essential for sorting into clathrin-coated pits and for downregulation of CD4

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Interaction of HIV-1 Nef with the cellular dileucine-based sorting pathway is required for CD4 down-regulation and optimal viral infectivity

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Importance of the nef gene for maintenance of high virus loads and for development of AIDS

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Apoptosis inhibitory activity of cytoplasmic p21(Cip1/WAF1) in monocytic differentiation

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Suppression of apoptosis signal-regulating kinase 1-induced cell death by 14-3-3 proteins

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Inhibition of the interferon-inducible protein kinase PKR by HCV E2 protein

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Inhibition of the mitogen-activated protein kinase kinase superfamily by a Yersinia effector

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