C
Charles Y. Lin
Researcher at Baylor College of Medicine
Publications - 128
Citations - 19573
Charles Y. Lin is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Transcription factor & Enhancer. The author has an hindex of 42, co-authored 116 publications receiving 15889 citations. Previous affiliations of Charles Y. Lin include Harvard University & University of California, San Diego.
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Journal ArticleDOI
Stabilization of the Max Homodimer with a Small Molecule Attenuates Myc-Driven Transcription.
Nicholas B. Struntz,Andrew Chen,Anja Deutzmann,Robert M. Wilson,Eric Stefan,Helen L. Evans,Maricela A. Ramirez,Tong Liang,Francisco Caballero,Mattheus H.E. Wildschut,Dylan V. Neel,David B. Freeman,Marius S. Pop,Marie McConkey,Marie McConkey,Marie McConkey,Sandrine Muller,Brice Harrison Curtin,Hanna Tseng,Kristen R. Frombach,Vincent L. Butty,Stuart S. Levine,Clementine Feau,Sarah Elmiligy,Jiyoung A. Hong,Jiyoung A. Hong,Timothy A. Lewis,Amedeo Vetere,Paul A. Clemons,Scott E. Malstrom,Benjamin L. Ebert,Benjamin L. Ebert,Benjamin L. Ebert,Charles Y. Lin,Dean W. Felsher,Angela N. Koehler +35 more
TL;DR: The asymmetric polycyclic lactam, KI-MS2-008, is discovered, which stabilizes the Max homodimer while reducing Myc protein and Myc-regulated transcript levels and supports altering Max dimerization as an alternative approach to targeting Myc.
Journal ArticleDOI
PI3K/AKT Signaling Regulates H3K4 Methylation in Breast Cancer
Jennifer M. Spangle,Koen M.A. Dreijerink,Anna C. Groner,Hailing Cheng,Carolynn E. Ohlson,Jaime M. Reyes,Charles Y. Lin,James E. Bradner,Jean J. Zhao,Thomas M. Roberts,Myles Brown +10 more
TL;DR: The data identify a mechanism by which PI3K/AKT signaling modulates the cancer epigenome through controlling H3K4 methylation and suggest that KDM5A subcellular localization and genome occupancy may be pharmacodynamic markers of the activity of PI3k/AKt inhibitors currently in clinical development.
Journal ArticleDOI
Spliceosome-targeted therapies trigger an antiviral immune response in triple-negative breast cancer
Elizabeth A. Bowling,Jarey H. Wang,Fade Gong,William Wu,Nicholas J. Neill,Ik Sun Kim,Siddhartha Tyagi,Mayra Orellana,Sarah J. Kurley,Rocio Dominguez-Vidana,Hsiang-Ching Chung,Tiffany Y.T. Hsu,Julien Dubrulle,Alexander B. Saltzman,Heyuan Li,Jitendra K. Meena,Gino M. Canlas,Srinivas Chamakuri,Swarnima Singh,Lukas M. Simon,Calla M. Olson,Lacey E. Dobrolecki,Michael T. Lewis,Bing Zhang,Ido Golding,Jeffrey M. Rosen,Damian W. Young,Anna Malovannaya,Fabio Stossi,George Miles,Matthew J. Ellis,Lihua Yu,Silvia Buonamici,Charles Y. Lin,Kristen L. Karlin,Xiang Zhang,Thomas F. Westbrook +36 more
TL;DR: It is discovered that mis-spliced RNA itself is a molecular trigger for tumor killing through viral mimicry, indicating that dsRNA-sensing pathways respond to global aberrations of RNA splicing in cancer and provoking the hypothesis that STTs may provide unexplored strategies to activate anti-tumor immune pathways.
Journal ArticleDOI
Signal-Dependent Recruitment of BRD4 to Cardiomyocyte Super-Enhancers Is Suppressed by a MicroRNA
Matthew S. Stratton,Charles Y. Lin,Priti Anand,Philip D. Tatman,Bradley S. Ferguson,Sean T. Wickers,Amrut V. Ambardekar,Carmen C. Sucharov,James E. Bradner,Saptarsi M. Haldar,Timothy A. McKinsey +10 more
TL;DR: It is suggested that dynamic enrichment of BRD4 at SEs genome-wide serves a crucial role in the control of stress-induced cardiac gene expression and is defined as a miR-dependent signaling mechanism for the regulation of chromatin state and Pol II phosphorylation.
Journal ArticleDOI
Discovery of a selective inhibitor of doublecortin like kinase 1
Fleur M. Ferguson,Behnam Nabet,Srivatsan Raghavan,Srivatsan Raghavan,Yan Liu,Alan L. Leggett,Miljan Kuljanin,Radha L. Kalekar,Radha L. Kalekar,Annan Yang,Annan Yang,Shuning He,Jinhua Wang,Raymond W.S. Ng,Raymond W.S. Ng,Rita Sulahian,Lianbo Li,Emily J. Poulin,Ling Huang,Jost Vrabic Koren,Nora Diéguez-Martínez,Sergio Espinosa,Zeng Zhiyang,Cesear Corona,James D Vasta,Ryoma Ohi,Taebo Sim,Nam Doo Kim,Wayne Harshbarger,Jose M. Lizcano,Matthew B. Robers,Senthil Muthaswamy,Senthil Muthaswamy,Charles Y. Lin,A. Thomas Look,A. Thomas Look,Kevin M. Haigis,Kevin M. Haigis,Joseph D. Mancias,Brian M. Wolpin,Brian M. Wolpin,Andrew J. Aguirre,Andrew J. Aguirre,Andrew J. Aguirre,William C. Hahn,William C. Hahn,William C. Hahn,Kenneth D. Westover,Nathanael S. Gray +48 more
TL;DR: A highly selective inhibitor of the DCLK1/2 kinases is used to uncover the consequences of D CLK1 inhibition on viability, phosphosignaling and the transcriptome in patient-derived organoid models of pancreatic ductal adenocarcinoma.