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HIV-1 Vpr protein activates the NF-κB pathway to promote G2/M cell cycle arrest

Liang, Zhibin ; Liu, Ruikang ; Lin, Yongquan ; Liang, Chen ; Tan, Juan ; Qiao, Wentao

Virologica Sinica, 2015-12, Vol.30 (6), p.441-448 [Periódico revisado por pares]

Wuhan: Wuhan Institute of Virology, CAS

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Título:
HIV-1 Vpr protein activates the NF-κB pathway to promote G2/M cell cycle arrest
Autor: Liang, Zhibin ; Liu, Ruikang ; Lin, Yongquan ; Liang, Chen ; Tan, Juan ; Qiao, Wentao
Assuntos: 1(HIV-1); viral ; arrest ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; cell cycle checkpoints ; DNA Replication ; G2 Phase Cell Cycle Checkpoints - physiology ; HEK293 Cells ; HeLa Cells ; HIV-1 - genetics ; HIV-1 - metabolism ; HIV-1 - physiology ; Host-Pathogen Interactions ; Human ; Human immunodeficiency virus 1 ; Humans ; immunodeficiency ; Medical Microbiology ; Microbial Genetics and Genomics ; Microbiology ; Models, Molecular ; mutants ; Mutation ; NF-kappa B - metabolism ; Oncology ; pathogenesis ; protein ; Protein Structure, Tertiary ; R(Vpr); NF-κB; G2/M ; Research Article ; reverse transcription ; Reverse Transcription - drug effects ; RNA Interference ; transcription factor NF-kappa B ; Transcriptional Activation ; type ; Virology ; virus ; Virus Replication ; vpr Gene Products, Human Immunodeficiency Virus - chemistry ; vpr Gene Products, Human Immunodeficiency Virus - genetics ; vpr Gene Products, Human Immunodeficiency Virus - metabolism
É parte de: Virologica Sinica, 2015-12, Vol.30 (6), p.441-448
Notas: 42-1760/Q
Zhibin Liang;Ruikang Liu;Yongquan Lin;Chen Liang;Juan Tan;Wentao Qiao;Key Laboratory of Molecular Microbiology and Biotechnology (Ministry of Education) and Key Laboratory of Microbial Functional Genomics (Tianjin), College of Life Sciences, Nankai University;Laboratory of Viral Diseases, NIAID, National Institutes of Health;Lady Davis Institute, Jewish General Hospital;Departments of Medicine, Mc Gill University;Department of Microbiology and Immunology, Mc Gill University
http://dx.doi.org/10.1007/s12250-015-3654-8
ObjectType-Article-1
SourceType-Scholarly Journals-1
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Descrição: Viral protein R (Vpr) plays an important role in the replication and pathogenesis of Human immunodeficiency virus type 1 (HIV-1). Some of the various functions attributed to Vpr, including the induction of G2/M cell cycle arrest, activating the NF-κB pathway, and promoting viral reverse transcription, might be interrelated. To test this hypothesis, a panel of Vpr mutants were investigated for their ability to induce G2/M arrest and to activate the NF-κB pathway. The results showed that the Vpr mutants that failed to activate NF-κB also lost the activity to induce G2/M arrest, which suggests that inducing G2/M arrest via Vpr depends at least partially on the activation of NF-κB. This latter possibility is supported by data showing that knocking down the key factors in the NF-κB pathway–p65, RelB, IKKα, or IKKβ–partially rescued the G2/M arrest induced by Vpr. Our results suggest that the NF-κB pathway is probably involved in Vpr-induced G2/M cell cycle arrest.
Editor: Wuhan: Wuhan Institute of Virology, CAS
Idioma: Inglês;Chinês

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HIV-1 Vpr protein activates the NF-κB pathway to promote G2/M cell cycle arrest

Liang, Zhibin ; Liu, Ruikang ; Lin, Yongquan ; Liang, Chen ; Tan, Juan ; Qiao, Wentao

Wuhan: Wuhan Institute of Virology, CAS

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