Author

Robert K Bradley

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cancer Biology· 2

Signature Assays, Organisms & Methods

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Organism:human· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Assay:multiome· 1 Approach:statistical model· 1 Assay:whole-exome sequencing· 1

Frequent Co-Authors

Ahmad S Zebari· 1 shared Aravind Ramakrishnan· 1 shared Brian Hayes· 1 shared Clara Kielkopf· 1 shared Dennis Liang Fei· 1 shared Harold Varmus· 1 shared Hayley Motowski· 1 shared Janine O Ilagan· 1 shared

Activity by Year

2014-2016 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 20 mutual co-author links

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1 shared paperCancer Biology

Ahmad S Zebari

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2 papers

Recent·Most cited

Wild-type U2AF1 antagonizes the splicing program characteristic of U2AF1-mutant tumors and is required for cell survival

Dennis Liang Fei, Hayley Motowski, Rakesh Chatrikhi, Sameer Prasad, Jovian Yu, Shaojian Gao, Clara Kielkopf, Robert K Bradley, Harold Varmus

The paper shows that wild-type U2AF1 counteracts the splicing changes caused by the S34F mutation in lung cancer and is essential for cell survival, while the mutant protein is not required for growth.

bioRxiv · Aug 24, 2016Cancer Biology

U2AF1 mutations alter splice site recognition in hematological malignancies

Janine O Ilagan, Aravind Ramakrishnan, Brian Hayes, Michele E Murphy, Ahmad S Zebari, Philip Bradley, Robert K Bradley

This study shows U2AF1 mutations alter 3' splice site recognition in hematological malignancies, affecting splicing of genes involved in DNA methylation, X inactivation, DNA damage response, and apoptosis.

bioRxiv · Sep 29, 2014Cancer Biology