YAP Drives Growth by Controlling Transcriptional Pause Release from Dynamic Enhancers
Molecular Cell, ISSN: 1097-2765, Vol: 60, Issue: 2, Page: 328-337
2015
- 217Citations
- 280Captures
- 1Mentions
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations217
- Citation Indexes217
- 217
- CrossRef86
- Captures280
- Readers280
- 280
- Mentions1
- Blog Mentions1
- Blog1
Article Description
The Hippo/YAP signaling pathway is a crucial regulator of tissue growth, stem cell activity, and tumorigenesis. However, the mechanism by which YAP controls transcription remains to be fully elucidated. Here, we utilize global chromatin occupancy analyses to demonstrate that robust YAP binding is restricted to a relatively small number of distal regulatory elements in the genome. YAP occupancy defines a subset of enhancers and superenhancers with the highest transcriptional outputs. YAP modulates transcription from these elements predominantly by regulating promoter-proximal polymerase II (Pol II) pause release. Mechanistically, YAP interacts and recruits the Mediator complex to enhancers, allowing the recruitment of the CDK9 elongating kinase. Genetic and chemical perturbation experiments demonstrate the requirement for Mediator and CDK9 in YAP-driven phenotypes of overgrowth and tumorigenesis. Our results here uncover the molecular mechanisms employed by YAP to exert its growth and oncogenic functions, and suggest strategies for intervention.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1097276515006978; http://dx.doi.org/10.1016/j.molcel.2015.09.001; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84944897345&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/26439301; https://linkinghub.elsevier.com/retrieve/pii/S1097276515006978
Elsevier BV
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