Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Human immunodeficiency virus type 1 Vpr modifies cell proliferation via multiple pathways.

T Yamaguchi1, N Watanabe, H Nakauchi

  • 1Department of Immunology, Institute of Basic Medical Sciences and Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Japan.

Microbiology and Immunology
|August 17, 1999
PubMed
Summary

The HIV-1 accessory protein Vpr inhibits cell proliferation across species, independent of its G2 cell cycle arrest function. This suggests a novel mechanism influencing fundamental cellular processes.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Diamond Blackfan anemia is mediated by hyperactive Nemo-like kinase.

Nature communications·2020
Same author

Inhibition of plasmin attenuates murine acute graft-versus-host disease mortality by suppressing the matrix metalloproteinase-9-dependent inflammatory cytokine storm and effector cell trafficking.

Leukemia·2014
Same author

Impaired hematopoietic differentiation of RUNX1-mutated induced pluripotent stem cells derived from FPD/AML patients.

Leukemia·2014
Same author

Haploinsufficiency of Sf3b1 leads to compromised stem cell function but not to myelodysplasia.

Leukemia·2014
Same author

Highly efficient generation of definitive endoderm lineage from human induced pluripotent stem cells.

Transplantation proceedings·2012
Same author

Plasmin inhibitor reduces T-cell lymphoid tumor growth by suppressing matrix metalloproteinase-9-dependent CD11b(+)/F4/80(+) myeloid cell recruitment.

Leukemia·2011

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • The HIV-1 accessory protein Vpr is known to arrest the cell cycle at the G2 phase.
  • Vpr-mediated G2 arrest is considered important for the HIV-1 viral life cycle.

Purpose of the Study:

  • To quantitatively assess Vpr-mediated cell cycle arrest using a bicistronic vector.
  • To investigate the effects of various Vpr proteins on cell cycle progression and growth in different species.

Main Methods:

  • Utilized a bicistronic vector encoding the vpr gene and green fluorescence protein for quantitative analysis.
  • Examined Vpr's impact on cell cycle progression and proliferation in HeLa, 293T, and monkey cell lines.
  • Analyzed chimeric Vpr proteins to identify regions responsible for species-non-specific activity.

Related Experiment Videos

Main Results:

  • Vpr2 (from HIV-1SF2 strain) induced G2 arrest in 293T cells but not significantly in HeLa cells.
  • Vpr2 strongly inhibited cell proliferation in both HeLa and 293T cells, as well as in monkey cells.
  • Chimeric Vpr analyses indicated that the C-terminal region alone does not mediate the species-non-specific growth inhibition.
  • Vpr's growth inhibitory activity was found to be independent of its G2 arresting activity.

Conclusions:

  • Vpr exhibits species-non-specific growth inhibitory activity.
  • This growth inhibition is independent of Vpr's ability to cause G2 cell cycle arrest.
  • Vpr may employ a novel mechanism to retard cell proliferation by affecting basic cellular functions.