ArticleJournal of virology2002
Expression of exogenous Sam68, the 68-kilodalton SRC-associated protein in mitosis, is able to alleviate impaired Rev function in astrocytes.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 53 citations in OpenAlex.
- HIV infection of non-classical cells in the brain.Retrovirology · 2023Review
- Review
- Morphine exposure exacerbates HIV-1 Tat driven changes to neuroinflammatory factors in cultured astrocytes.PloS one · 2020Article
- Nef is secreted in exosomes from Nef.GFP-expressing and HIV-1-infected human astrocytes.Journal of neurovirology · 2017Article
- Astrocytes as an HIV Reservoir: Mechanism of HIV Infection.Current HIV research · 2016Review
- Analysis of the interaction between host factor Sam68 and viral elements during foot-and-mouth disease virus infections.Virology journal · 2015Article
- Cell-cell contact viral transfer contributes to HIV infection and persistence in astrocytes.Journal of neurovirology · 2015Article
- STAT3 and its phosphorylation are involved in HIV-1 Tat-induced transactivation of glial fibrillary acidic protein.Current HIV research · 2015Article
- Interplay between Wnt/β-catenin signaling and HIV: virologic and biologic consequences in the CNS.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012Review
- Human immunodeficiency virus type 1 (HIV-1) transactivator of transcription through its intact core and cysteine-rich domains inhibits Wnt/β-catenin signaling in astrocytes: relevance to HIV neuropathogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Hsp22 (HspB8/H11) knockdown induces Sam68 expression and stimulates proliferation of glioblastoma cells.Journal of cellular physiology · 2011Article
- Translational regulation of HIV-1 replication by HIV-1 Rev cellular cofactors Sam68, eIF5A, hRIP, and DDX3.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011Article
- Article
- Structural basis for homodimerization of the Src-associated during mitosis, 68-kDa protein (Sam68) Qua1 domain.The Journal of biological chemistry · 2010Article
- Sam68 relocalization into stress granules in response to oxidative stress through complexing with TIA-1.Experimental cell research · 2009Article
- Inhibition of HIV-1 entry by extracts derived from traditional Chinese medicinal herbal plants.BMC complementary and alternative medicine · 2009Article
- Suppression of HIV-1 Nef translation by Sam68 mutant-induced stress granules and nef mRNA sequestration.Molecular cell · 2009Article
- Human immunodeficiency virus-restricted replication in astrocytes and the ability of gamma interferon to modulate this restriction are regulated by a downstream effector of the Wnt signaling pathway.Journal of virology · 2007Article
- Low TRBP levels support an innate human immunodeficiency virus type 1 resistance in astrocytes by enhancing the PKR antiviral response.Journal of virology · 2005Article
- A novel function for Sam68: enhancement of HIV-1 RNA 3' end processing.RNA (New York, N.Y.) · 2004Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Human immunodeficiency virus type 1 (HIV-1) gene expression in astrocytes is restricted, resulting in a brief and limited synthesis of HIV-1 viral structural proteins. Impaired Rev function has been documented in these cells. However, the molecular mechanisms underlying the impaired Rev function are not fully understood. Using the astroglial cell line U87.MG as a model, we report here that HIV-1 gene expression down-regulated expression of Sam68, the 68-kDa Src-associated protein in mitosis, which was constitutively expressed at a lower level in astrocytes. Elevating the endogenous level of Sam68 expression considerably restored HIV-1 Rev function in astrocytes, as determined by a Rev-dependent reporter gene assay. However, elevation of Sam68 expression achieved only a modest increase in HIV-1 production, further supporting the notion that there are multiple cellular restrictions of HIV-1 gene expression in astrocytes. Mutagenesis analysis identified the region between amino acids 321 and 410 of Sam68 as being directly involved in the binding of Sam68 to Rev, while a double mutation in Rev, L78D and E79L, like those in the dominant-negative Rev mutant M10, eliminated Rev binding to Sam68. Moreover, subcellular fractionation and digital fluorescence microscopic imaging revealed that Sam68 expression promoted Rev nuclear export. Taken together, our studies demonstrate that a lower level of constitutive Sam68 expression, followed by further down-regulation by HIV-1 infection, contributes to impaired Rev function in astrocytes, and they suggest that Sam68 may play an important role in Rev nuclear export.
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