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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Cancer cells display high levels of oncogene-induced replication stress (RS) and rely on DNA damage checkpoint for viability. This feature is exploited by cancer therapies to either increase RS to unbearable levels or inhibit checkpoint kinases involved in the DNA damage response. Thus far, treatments that combine these two strategies have shown promise but also have severe adverse effects. To identify novel, better-tolerated anticancer combinations, we screened a collection of plant extracts and found two natural compounds from the plant, Psoralea corylifolia, that synergistically inhibit cancer cell proliferation. Bakuchiol inhibited DNA replication and activated the checkpoint kinase CHK1 by targeting DNA polymerases. Isobavachalcone interfered with DNA double-strand break repair by inhibiting the checkpoint kinase CHK2 and DNA end resection. The combination of bakuchiol and isobavachalcone synergistically inhibited cancer cell proliferation in vitro. Importantly, it also prevented tumor development in xenografted NOD/SCID mice. The synergistic effect of inhibiting DNA replication and CHK2 signaling identifies a vulnerability of cancer cells that might be exploited by using clinically approved inhibitors in novel combination therapies.
