ArticleMolecular and cellular biology2006
Human immunodeficiency virus type 1 Vpr induces G2 checkpoint activation by interacting with the splicing factor SAP145.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Tyramide signal amplification mass spectrometry (TSA-MS) ratio identifies nuclear speckle proteins.The Journal of cell biology · 2020Article
- The SF3b complex: splicing and beyond.Cellular and molecular life sciences : CMLS · 2020Review
- The Severe Fever with Thrombocytopenia Syndrome Virus NSs Protein Interacts with CDK1 To Induce GJournal of virology · 2020Article
- Review
- Promiscuous Targeting of Cellular Proteins by Vpr Drives Systems-Level Proteomic Remodeling in HIV-1 Infection.Cell reports · 2019Article
- Genome-Wide CRISPR Screen for Essential Cell Growth Mediators in Mutant KRAS Colorectal Cancers.Cancer research · 2017Article
- Solution structure of the first RNA recognition motif domain of human spliceosomal protein SF3b49 and its mode of interaction with a SF3b145 fragment.Protein science : a publication of the Protein Society · 2017Article
- Can the HIV-1 splicing machinery be targeted for drug discovery?HIV/AIDS (Auckland, N.Z.) · 2017Review
- Unique Features of Human Protein Arginine Methyltransferase 9 (PRMT9) and Its Substrate RNA Splicing Factor SF3B2.The Journal of biological chemistry · 2015Article
- PRMT9 is a type II methyltransferase that methylates the splicing factor SAP145.Nature communications · 2015Article
- A systems biology examination of the human female genital tract shows compartmentalization of immune factor expression.Journal of virology · 2013Article
- Expression profile of genes involved in pathogenesis of pediatric Crohn's disease.Journal of gastroenterology and hepatology · 2012Article
- HIV-1 Vpr loads uracil DNA glycosylase-2 onto DCAF1, a substrate recognition subunit of a cullin 4A-ring E3 ubiquitin ligase for proteasome-dependent degradation.The Journal of biological chemistry · 2010Article
- Identification of host proteins associated with HIV-1 preintegration complexes isolated from infected CD4+ cells.Retrovirology · 2010Article
- The DNA unwinding element binding protein DUE-B interacts with Cdc45 in preinitiation complex formation.Molecular and cellular biology · 2010Article
- HIV-1 Vpr: mechanisms of G2 arrest and apoptosis.Experimental and molecular pathology · 2008Review
- Feline immunodeficiency virus OrfA alters gene expression of splicing factors and proteasome-ubiquitination proteins.Virology · 2008Article
- G2/M cell cycle arrest in the life cycle of viruses.Virology · 2007Review
- Vpr is required for efficient Nef expression from unintegrated human immunodeficiency virus type 1 DNA.Journal of virology · 2007Article
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vpr, the viral protein R of human immunodeficiency virus type 1, induces G(2) cell cycle arrest and apoptosis in mammalian cells via ATR (for "ataxia-telangiectasia-mediated and Rad3-related") checkpoint activation. The expression of Vpr induces the formation of the gamma-histone 2A variant X (H2AX) and breast cancer susceptibility protein 1 (BRCA1) nuclear foci, and a C-terminal domain is required for Vpr-induced ATR activation and its nuclear localization. However, the cellular target of Vpr, as well as the mechanism of G(2) checkpoint activation, was unknown. Here we report that Vpr induces checkpoint activation and G(2) arrest by binding to the CUS1 domain of SAP145 and interfering with the functions of the SAP145 and SAP49 proteins, two subunits of the multimeric splicing factor 3b (SF3b). Vpr interacts with and colocalizes with SAP145 through its C-terminal domain in a speckled distribution. The depletion of either SAP145 or SAP49 leads to checkpoint-mediated G(2) cell cycle arrest through the induction of nuclear foci containing gamma-H2AX and BRCA1. In addition, the expression of Vpr excludes SAP49 from the nuclear speckles and inhibits the formation of the SAP145-SAP49 complex. To conclude, these results point out the unexpected roles of the SAP145-SAP49 splicing factors in cell cycle progression and suggest that cellular expression of Vpr induces checkpoint activation and G(2) arrest by interfering with the function of SAP145-SAP49 complex in host cells.
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