ArticleCell cycle (Georgetown, Tex.)2010
Mutation of the DEAD-box helicase belle downregulates the cyclin-dependent kinase inhibitor Dacapo.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- TheCells · 2020Article
- RNA helicase Belle/DDX3 regulates transgene expression in Drosophila.Developmental biology · 2016Article
- NAT1/DAP5/p97 and atypical translational control in the Drosophila Circadian Oscillator.Genetics · 2012Article
- The microRNA pathway regulates the temporal pattern of Notch signaling in Drosophila follicle cells.Development (Cambridge, England) · 2011Article
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
The retinoblastoma protein (pRB) negatively regulates cell proliferation by limiting the activity of the family of E2F transcription factors. In Drosophila, mutation of the DEAD-box helicase belle (bel) relieves an E2F/pRB induced G(1) cell cycle arrest; however, the mechanism of this rescue is unknown. Here, we show that the level of the cyclin-dependent kinase inhibitor Dacapo (Dap), homolog of mammalian p21/p27, is strongly reduced both in bel mutant cells in vivo and in tissue culture cells depleted of Bel by RNA interference. Interestingly, the loss of bel also partially alleviates an ectopically induced G(1) cell cycle arrest. Additionally, we show that Bel undergoes nucleocytoplasmic shuttling. Thus, inactivation of bel renders cells less sensitive to several anti-proliferative signals inducing G(1) arrest.
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