Journal
JOURNAL OF VIROLOGY
Volume 77, Issue 3, Pages 2063-2070Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.77.3.2063-2070.2003
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Funding
- NCI NIH HHS [R01 CA070018, CA70018] Funding Source: Medline
- NIAID NIH HHS [R01 AI039975, R01 AI043190, AI39975, AI43190] Funding Source: Medline
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Human immunodeficiency virus (HIV) protein R (Vpr) induces G(2) arrest, and prolonged G(2) arrest leads to apoptosis. We find that in HeLa cells the cell cycle regulatory kinase, Wee-1, is depleted following prolonged G(2) arrest induced by Vpr. Of note, small interfering RNAs directed to Wee-1 triggered apoptosis, suggesting a direct role for Wee-1 in apoptosis. In support of this hypothesis, overexpression of Wee-1 suppressed Vpr-mediated apoptosis. Importantly, similar results were observed with cells induced to undergo apoptosis gamma irradiation. Thus, Wee-1 may serve as a key regulator of both HIV type I Vpr- and gamma irradiation-mediated apoptosis and possibly serve as a general regulator linking the cell cycle to some pathways of apoptosis.
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