How open science helps researchers succeed
- National Autonomous University of Mexico, Mexico
- National Institutes of Health, United States
- University of California, Davis, United States
- Laura and John Arnold Foundation, United States
- BioMed Central, United Kingdom
- CrossRef, United Kingdom
- University of Texas at Austin, United States
- Center for Open Science, United States
- University of California, Berkeley, United States
- Mozilla Foundation, United States
- Gesmer Updegrove LLP, United States
- Washington State University, United States
Abstract
Open access, open data, open source, and other open scholarship practices are growing in popularity and necessity. However, widespread adoption of these practices has not yet been achieved. One reason is that researchers are uncertain about how sharing their work will affect their careers. We review literature demonstrating that open research is associated with increases in citations, media attention, potential collaborators, job opportunities, and funding opportunities. These findings are evidence that open research practices bring significant benefits to researchers relative to more traditional closed practices.
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© 2016, McKiernan et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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How open science helps researchers succeed
eLife 5:e16800.
https://doi.org/10.7554/eLife.16800
Further reading
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Researchers can benefit from making their research findings freely available online.
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- Biochemistry and Chemical Biology
In healthy cells, cyclin D1 is expressed during the G1 phase of the cell cycle, where it activates CDK4 and CDK6. Its dysregulation is a well-established oncogenic driver in numerous human cancers. The cancer-related function of cyclin D1 has been primarily studied by focusing on the phosphorylation of the retinoblastoma (RB) gene product. Here, using an integrative approach combining bioinformatic analyses and biochemical experiments, we show that GTSE1 (G-Two and S phases expressed protein 1), a protein positively regulating cell cycle progression, is a previously unrecognized substrate of cyclin D1–CDK4/6 in tumor cells overexpressing cyclin D1 during G1 and subsequent phases. The phosphorylation of GTSE1 mediated by cyclin D1–CDK4/6 inhibits GTSE1 degradation, leading to high levels of GTSE1 across all cell cycle phases. Functionally, the phosphorylation of GTSE1 promotes cellular proliferation and is associated with poor prognosis within a pan-cancer cohort. Our findings provide insights into cyclin D1’s role in cell cycle control and oncogenesis beyond RB phosphorylation.
