Rafael E. Herrera
Stanford University
12 Papers
1 Citations
Rafael E. Herrera is an academic researcher from Stanford University. The author has contributed to research in topics: Histone code & Histone H1. The author has an hindex of 9, co-authored 11 publications. Previous affiliations of Rafael E. Herrera include Baylor College of Medicine & University of Texas Health Science Center at San Antonio.
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Papers
Forkhead Homologue in Rhabdomyosarcoma Functions as a Bifunctional Nuclear Receptor-interacting Protein with Both Coactivator and Corepressor Functions
Holly Hong Zhao,Rafael E. Herrera,Rafael E. Herrera,Ester Coronado-Heinsohn,Michael C. Yang,John H. Ludes-Meyers,Karen J. Seybold-Tilson,Zafar Nawaz,Douglas Yee,Frederic G. Barr,Sami Diab,Powel H. Brown,Powel H. Brown,Suzanne A. W. Fuqua,Suzanne A. W. Fuqua,C. Kent Osborne,C. Kent Osborne +16 more
TL;DR: In conclusion, overexpression of FKHR dramatically inhibits the proliferation of ER-dependent MCF-7 breast cancer cells and represents a bifunctional NR intermediary protein that can act as either a coactivator or corepressor, depending on the receptor type.
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Somatic mutation distributions in cancer genomes vary with three-dimensional chromatin structure
Kadir C. Akdemir,Victoria T. Le,Justin M. Kim,Justin M. Kim,Sarah Killcoyne,Sarah Killcoyne,Devin A. King,Ya-Ping Lin,Yanyan Tian,Akira Inoue,Samirkumar B. Amin,Frederick S. Robinson,Manjunath Nimmakayalu,Rafael E. Herrera,Erica Lynn,Kin Chan,Kin Chan,Sahil Seth,Leszek J. Klimczak,Moritz Gerstung,Dmitry A. Gordenin,John P. O'Brien,Lei Li,Yonathan Lissanu Deribe,Roel G.W. Verhaak,Peter J. Campbell,Rebecca C. Fitzgerald,Ashby J. Morrison,Jesse R. Dixon,P. Andrew Futreal +29 more
TL;DR: The analyses reveal that the change in somatic mutational load in cancer genomes is co-localized with topologically-associating-domain boundaries, and the interplay between three-dimensional genome organization and active mutational processes has a substantial influence on the large-scale mutation-rate variations observed in human cancers.
Carcinogen susceptibility is regulated by genome architecture and predicts cancer mutagenesis
Pablo E. García-Nieto,Erin K. Schwartz,Devin A. King,Jonas Paulsen,Philippe Collas,Rafael E. Herrera,Ashby J. Morrison +6 more
TL;DR: This study presents the first quantitative human genome‐wide map of DNA lesions induced by ultraviolet (UV) radiation, the ubiquitous carcinogen in sunlight that causes skin cancer, and identifies carcinogen susceptibility as an origin of genome instability that is regulated by nuclear architecture and mirrors mutagenesis in cancer.
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Genome-wide profiles of UV lesion susceptibility, repair, and mutagenic potential in melanoma.
Brian S. Perez,Ka Man Wong,Erin K. Schwartz,Rafael E. Herrera,Devin A. King,Pablo E. García-Nieto,Ashby J. Morrison +6 more
TL;DR: In this article, the authors compared genome-wide maps of 6-4PP and CPD lesion abundances in primary cells and conducted comprehensive analyses to determine the genetic and epigenetic features associated with susceptibility.
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Process-specific somatic mutation distributions vary with three-dimensional genome structure
Kadir C. Akdemir,Victoria T. Le,Sarah Killcoyne,Devin A. King,Yongsheng Li,Yanyan Tian,Akira Inoue,Samirkumar B. Amin,Frederick S. Robinson,Rafael E. Herrera,Erica Lynn,Kin Chan,Sahil Seth,Leszek J. Klimczak,Moritz Gerstung,Dmitry A. Gordenin,John P. O'Brien,Lei Li,Roeland Verhaak,Peter J. Campbell,Rebecca C. Fitzgerald,Ashby J. Morrison,Dixon,Andrew Futreal P +23 more
TL;DR: A study of 3000 tumor-normal pair whole genome datasets from more than 40 different human cancer types revealed that different mutational processes lead to distinct somatic mutation distributions between chromatin folding domains, and it was shown that mutational distributions shift during cancer evolution upon mutational process switch.