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2. Obesity-linked suppression of membrane-bound O-acyltransferase 7 (MBOAT7) drives non-alcoholic fatty liver disease.

Author

Helsley, Robert, Varadharajan, Venkateshwari, Brown, Amanda, Gromovsky, Anthony, Schugar, Rebecca, Ramachandiran, Iyappan, Fung, Kevin, Kabbany, Mohammad, Banerjee, Rakhee, Neumann, Chase, Finney, Chelsea, Pathak, Preeti, Orabi, Danny, Osborn, Lucas, Massey, William, Zhang, Renliang, Kadam, Anagha, Sansbury, Brian, Pan, Calvin, Sacks, Jessica, Lee, Richard, Crooke, Rosanne, Graham, Mark, Lemieux, Madeleine, Gogonea, Valentin, Kirwan, John, Allende, Daniela, Civelek, Mete, Fox, Paul, Rudel, Lawrence, Lusis, Aldons, Spite, Matthew, and Brown, J

Subjects
NAFLD, hepatology, human biology, medicine, mouse, triacylglycerol, Acylation, Acyltransferases, Animals, Disease Progression, Humans, Membrane Proteins, Mice, Non-alcoholic Fatty Liver Disease, Obesity
Abstract

Recent studies have identified a genetic variant rs641738 near two genes encoding membrane bound O-acyltransferase domain-containing 7 (MBOAT7) and transmembrane channel-like 4 (TMC4) that associate with increased risk of non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), alcohol-related cirrhosis, and liver fibrosis in those infected with viral hepatitis (Buch et al., 2015; Mancina et al., 2016; Luukkonen et al., 2016; Thabet et al., 2016; Viitasalo et al., 2016; Krawczyk et al., 2017; Thabet et al., 2017). Based on hepatic expression quantitative trait loci analysis, it has been suggested that MBOAT7 loss of function promotes liver disease progression (Buch et al., 2015; Mancina et al., 2016; Luukkonen et al., 2016; Thabet et al., 2016; Viitasalo et al., 2016; Krawczyk et al., 2017; Thabet et al., 2017), but this has never been formally tested. Here we show that Mboat7 loss, but not Tmc4, in mice is sufficient to promote the progression of NAFLD in the setting of high fat diet. Mboat7 loss of function is associated with accumulation of its substrate lysophosphatidylinositol (LPI) lipids, and direct administration of LPI promotes hepatic inflammatory and fibrotic transcriptional changes in an Mboat7-dependent manner. These studies reveal a novel role for MBOAT7-driven acylation of LPI lipids in suppressing the progression of NAFLD.

Published
2019

3. Dynamic Chromatin Targeting of BRD4 Stimulates Cardiac Fibroblast Activation

Author

Stratton, Matthew S, Bagchi, Rushita A, Felisbino, Marina B, Hirsch, Rachel A, Smith, Harrison E, Riching, Andrew S, Enyart, Blake Y, Koch, Keith A, Cavasin, Maria A, Alexanian, Michael, Song, Kunhua, Qi, Jun, Lemieux, Madeleine E, Srivastava, Deepak, Lam, Maggie PY, Haldar, Saptarsi M, Lin, Charles Y, and McKinsey, Timothy A

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Cardiovascular, Genetics, Heart Disease, Aetiology, 2.1 Biological and endogenous factors, Underpinning research, 1.1 Normal biological development and functioning, Animals, Azepines, Cell Adhesion Molecules, Cells, Cultured, Chromatin, Enhancer Elements, Genetic, Epigenesis, Genetic, Extracellular Matrix, Female, Fibrosis, Heart Failure, Heart Ventricles, Intracellular Signaling Peptides and Proteins, Male, Mice, Mice, Inbred C57BL, Myofibroblasts, Nuclear Proteins, Protein Binding, RNA Polymerase II, Rats, Rats, Sprague-Dawley, Transcription Factors, Transcriptome, Transforming Growth Factor beta, Triazoles, p38 Mitogen-Activated Protein Kinases, chromatin, fibroblast, heart failure, mass spectrometry, phenotype, signaling, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

RationaleSmall molecule inhibitors of the acetyl-histone binding protein BRD4 have been shown to block cardiac fibrosis in preclinical models of heart failure (HF). However, since the inhibitors target BRD4 ubiquitously, it is unclear whether this chromatin reader protein functions in cell type-specific manner to control pathological myocardial fibrosis. Furthermore, the molecular mechanisms by which BRD4 stimulates the transcriptional program for cardiac fibrosis remain unknown.ObjectiveWe sought to test the hypothesis that BRD4 functions in a cell-autonomous and signal-responsive manner to control activation of cardiac fibroblasts, which are the major extracellular matrix-producing cells of the heart.Methods and resultsRNA-sequencing, mass spectrometry, and cell-based assays employing primary adult rat ventricular fibroblasts demonstrated that BRD4 functions as an effector of TGF-β (transforming growth factor-β) signaling to stimulate conversion of quiescent cardiac fibroblasts into Periostin (Postn)-positive cells that express high levels of extracellular matrix. These findings were confirmed in vivo through whole-transcriptome analysis of cardiac fibroblasts from mice subjected to transverse aortic constriction and treated with the small molecule BRD4 inhibitor, JQ1. Chromatin immunoprecipitation-sequencing revealed that BRD4 undergoes stimulus-dependent, genome-wide redistribution in cardiac fibroblasts, becoming enriched on a subset of enhancers and super-enhancers, and leading to RNA polymerase II activation and expression of downstream target genes. Employing the Sertad4 (SERTA domain-containing protein 4) locus as a prototype, we demonstrate that dynamic chromatin targeting of BRD4 is controlled, in part, by p38 MAPK (mitogen-activated protein kinase) and provide evidence of a critical function for Sertad4 in TGF-β-mediated cardiac fibroblast activation.ConclusionsThese findings define BRD4 as a central regulator of the pro-fibrotic cardiac fibroblast phenotype, establish a p38-dependent signaling circuit for epigenetic reprogramming in heart failure, and uncover a novel role for Sertad4. The work provides a mechanistic foundation for the development of BRD4 inhibitors as targeted anti-fibrotic therapies for the heart.

Published
2019

5. BET bromodomain inhibition suppresses innate inflammatory and profibrotic transcriptional networks in heart failure.

Author

Duan, Qiming, McMahon, Sarah, Anand, Priti, Shah, Hirsh, Thomas, Sean, Salunga, Hazel, Huang, Yu, Zhang, Rongli, Sahadevan, Aarathi, Lemieux, Madeleine, Brown, Jonathan, Bradner, James, McKinsey, Timothy, Srivastava, Deepak, and Haldar, Saptarsi

Subjects
Animals, Azepines, Cardiomegaly, Gene Regulatory Networks, Heart Failure, Humans, Induced Pluripotent Stem Cells, Inflammation, Male, Mice, Mice, Inbred C57BL, Myocytes, Cardiac, NF-kappa B, Proteins, Signal Transduction, Transforming Growth Factor beta, Triazoles
Abstract

Despite current standard of care, the average 5-year mortality after an initial diagnosis of heart failure (HF) is about 40%, reflecting an urgent need for new therapeutic approaches. Previous studies demonstrated that the epigenetic reader protein bromodomain-containing protein 4 (BRD4), an emerging therapeutic target in cancer, functions as a critical coactivator of pathologic gene transactivation during cardiomyocyte hypertrophy. However, the therapeutic relevance of these findings to human disease remained unknown. We demonstrate that treatment with the BET bromodomain inhibitor JQ1 has therapeutic effects during severe, preestablished HF from prolonged pressure overload, as well as after a massive anterior myocardial infarction in mice. Furthermore, JQ1 potently blocks agonist-induced hypertrophy in human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). Integrated transcriptomic analyses across animal models and human iPSC-CMs reveal that BET inhibition preferentially blocks transactivation of a common pathologic gene regulatory program that is robustly enriched for NFκB and TGF-β signaling networks, typified by innate inflammatory and profibrotic myocardial genes. As predicted by these specific transcriptional mechanisms, we found that JQ1 does not suppress physiological cardiac hypertrophy in a mouse swimming model. These findings establish that pharmacologically targeting innate inflammatory and profibrotic myocardial signaling networks at the level of chromatin is effective in animal models and human cardiomyocytes, providing the critical rationale for further development of BET inhibitors and other epigenomic medicines for HF.

Published
2017

6. Glucocorticoids enhance muscle endurance and ameliorate Duchenne muscular dystrophy through a defined metabolic program

Author

Morrison-Nozik, Alexander, Anand, Priti, Zhu, Han, Duan, Qiming, Sabeh, Mohamad, Prosdocimo, Domenick A, Lemieux, Madeleine E, Nordsborg, Nikolai, Russell, Aaron P, MacRae, Calum A, Gerber, Anthony N, Jain, Mukesh K, and Haldar, Saptarsi M

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Genetics, Muscular Dystrophy, Pediatric, Rare Diseases, Intellectual and Developmental Disabilities (IDD), Duchenne/ Becker Muscular Dystrophy, Brain Disorders, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Musculoskeletal, Animals, Female, Glucocorticoids, Humans, Kruppel-Like Transcription Factors, Male, Mice, Mice, Inbred C57BL, Muscle, Skeletal, Muscular Dystrophy, Duchenne, Nuclear Proteins, Receptors, Glucocorticoid, skeletal muscle metabolism, glucocorticoid, exercise, Duchenne muscular dystrophy, steroid hormone nuclear receptor
Abstract

Classic physiology studies dating to the 1930s demonstrate that moderate or transient glucocorticoid (GC) exposure improves muscle performance. The ergogenic properties of GCs are further evidenced by their surreptitious use as doping agents by endurance athletes and poorly understood efficacy in Duchenne muscular dystrophy (DMD), a genetic muscle-wasting disease. A defined molecular basis underlying these performance-enhancing properties of GCs in skeletal muscle remains obscure. Here, we demonstrate that ergogenic effects of GCs are mediated by direct induction of the metabolic transcription factor KLF15, defining a downstream pathway distinct from that resulting in GC-related muscle atrophy. Furthermore, we establish that KLF15 deficiency exacerbates dystrophic severity and muscle GC-KLF15 signaling mediates salutary therapeutic effects in the mdx mouse model of DMD. Thus, although glucocorticoid receptor (GR)-mediated transactivation is often associated with muscle atrophy and other adverse effects of pharmacologic GC administration, our data define a distinct GR-induced gene regulatory pathway that contributes to therapeutic effects of GCs in DMD through proergogenic metabolic programming.

Published
2015

7. A chromosome-level genome of Astyanax mexicanus surface fish for comparing population-specific genetic differences contributing to trait evolution

Author

Warren, Wesley C., Boggs, Tyler E., Borowsky, Richard, Carlson, Brian M., Ferrufino, Estephany, Gross, Joshua B., Hillier, LaDeana, Hu, Zhilian, Keene, Alex C., Kenzior, Alexander, Kowalko, Johanna E., Tomlinson, Chad, Kremitzki, Milinn, Lemieux, Madeleine E., Graves-Lindsay, Tina, McGaugh, Suzanne E., Miller, Jeffrey T., Mommersteeg, Mathilda T. M., Moran, Rachel L., Peuß, Robert, Rice, Edward S., Riddle, Misty R., Sifuentes-Romero, Itzel, Stanhope, Bethany A., Tabin, Clifford J., Thakur, Sunishka, Yamamoto, Yoshiyuki, and Rohner, Nicolas

Published
2021
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8. BPTF regulates growth of adult and pediatric high-grade glioma through the MYC pathway

Author

Green, Adam L., DeSisto, John, Flannery, Patrick, Lemma, Rakeb, Knox, Aaron, Lemieux, Madeleine, Sanford, Bridget, O’Rourke, Rebecca, Ramkissoon, Shakti, Jones, Kristen, Perry, Jennifer, Hui, Xu, Moroze, Erin, Balakrishnan, Ilango, O’Neill, Allison F., Dunn, Katherine, DeRyckere, Deborah, Danis, Etienne, Safadi, Aaron, Gilani, Ahmed, Hubbell-Engler, Benjamin, Nuss, Zachary, Levy, Jean M. Mulcahy, Serkova, Natalie, Venkataraman, Sujatha, Graham, Douglas K., Foreman, Nicholas, Ligon, Keith, Jones, Ken, Kung, Andrew L., and Vibhakar, Rajeev

Published
2020
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9. Substrate stiffness modulates cardiac fibroblast activation, senescence, and proinflammatory secretory phenotypeSubstrate stiffness modulates cardiac fibroblast activation, senescence, and proinflammatory secretory phenotype.

Author

Felisbino, Marina B., Rubino, Marcello, Travers, Joshua G., Schuetze, Katherine B., Lemieux, Madeleine E., Anseth, Kristi S., Aguado, Brian A., and McKinsey, Timothy A.

Subjects
FIBROBLASTS, HEART cells, ETHYLENE glycol, HEART fibrosis, PHENOTYPES
Abstract

In vitro cultures of primary cardiac fibroblasts (CFs), the major extracellular matrix (ECM)-producing cells of the heart, are used to determine molecular mechanisms of cardiac fibrosis. However, the supraphysiologic stiffness of tissue culture polystyrene (TCPS) triggers the conversion of CFs into an activated myofibroblast-like state, and serial passage of the cells results in the induction of replicative senescence. These phenotypic switches confound the interpretation of experimental data obtained with cultured CFs. In an attempt to circumvent TCPS-induced activation and senescence of CFs, we used poly(ethylene glycol) (PEG) hydrogels as cell culture platforms with low and high stiffness formulations to mimic healthy and fibrotic hearts, respectively. Low hydrogel stiffness converted activated CFs into a quiescent state with a reduced abundance of a-smooth muscle actin (a-SMA)-containing stress fibers. Unexpectedly, lower substrate stiffness concomitantly augmented CF senescence, marked by elevated senescence-associated b-galactosidase (SA-b-Gal) activity and increased expression of p16 and p21, which are antiproliferative markers of senescence. Using dynamically stiffening hydrogels with phototunable cross-linking capabilities, we demonstrate that premature, substrate-induced CF senescence is partially reversible. RNA-sequencing analysis revealed widespread transcriptional reprogramming of CFs cultured on low-stiffness hydrogels, with a reduction in the expression of profibrotic genes encoding ECM proteins, and an attendant increase in expression of NF-κB-responsive inflammatory genes that typify the senescence-associated secretory phenotype (SASP). Our findings demonstrate that alterations in matrix stiffness profoundly impact CF cell state transitions, and suggest mechanisms by which CFs change phenotype in vivo depending on the stiffness of the myocardial microenvironment in which they reside. [ABSTRACT FROM AUTHOR]

Published
2024
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10. EZH2 Cooperates with BRD4-NUT to Drive NUT Carcinoma Growth by Silencing Key Tumor Suppressor Genes

Author

Huang, Yeying, primary, Durall, R. Taylor, additional, Luong, Nhi M., additional, Hertzler, Hans J., additional, Huang, Julianna, additional, Gokhale, Prafulla C., additional, Leeper, Brittaney A., additional, Persky, Nicole S., additional, Root, David E., additional, Anekal, Praju V., additional, Montero Llopis, Paula D.L.M., additional, David, Clement N., additional, Kutok, Jeffery L., additional, Raimondi, Alejandra, additional, Saluja, Karan, additional, Luo, Jia, additional, Zahnow, Cynthia A., additional, Adane, Biniam, additional, Stegmaier, Kimberly, additional, Hawkins, Catherine E., additional, Ponne, Christopher, additional, Le, Quan, additional, Shapiro, Geoffrey I., additional, Lemieux, Madeleine E., additional, Eagen, Kyle P., additional, and French, Christopher A., additional

Published
2023
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12. EZH2 synergizes with BRD4-NUT to drive NUT carcinoma growth through silencing of key tumor suppressor genes

Author

Huang, Yeying, primary, Durall, R Taylor, additional, Luong, Nhi M, additional, Hertzler, Hans J, additional, Huang, Julianna, additional, Gokhale, Prafulla C, additional, Leeper, Brittaney A, additional, Persky, Nicole S, additional, Root, David E, additional, Anekal, Praju V, additional, Montero Llopis, Paula DLM, additional, David, Clement N, additional, Kutok, Jeffery L, additional, Raimondi, Alejandra, additional, Saluja, Karan, additional, Luo, Jia, additional, Zahnow, Cynthia A, additional, Adane, Biniam, additional, Stegmaier, Kimberly, additional, Hawkins, Catherine E, additional, Ponne, Christopher, additional, Le, Quan, additional, Shapiro, Geoffrey I, additional, Lemieux, Madeleine E, additional, Eagen, Kyle P, additional, and French, Christopher A, additional

Published
2023
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14. Supplemental Figures from Combined Targeting of the BRD4–NUT–p300 Axis in NUT Midline Carcinoma by Dual Selective Bromodomain Inhibitor, NEO2734

Author

Morrison-Smith, Chevaun D., primary, Knox, Tatiana M., primary, Filic, Ivona, primary, Soroko, Kara M., primary, Eschle, Benjamin K., primary, Wilkens, Margaret K., primary, Gokhale, Prafulla C., primary, Giles, Francis, primary, Griffin, Andrew, primary, Brown, Bill, primary, Shapiro, Geoffrey I., primary, Zucconi, Beth E., primary, Cole, Philip A., primary, Lemieux, Madeleine E., primary, and French, Christopher A., primary

Published
2023
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15. Data from Chemical Screen Identifies Diverse and Novel Histone Deacetylase Inhibitors as Repressors of NUT Function: Implications for NUT Carcinoma Pathogenesis and Treatment

Author

Shiota, Hitoshi, primary, Alekseyenko, Artyom A., primary, Wang, Zhipeng A., primary, Filic, Ivona, primary, Knox, Tatiana M., primary, Luong, Nhi M., primary, Huang, Yeying, primary, Scott, David A., primary, Jones, Kristen L., primary, Gokhale, Prafulla C., primary, Lemieux, Madeleine E., primary, Cole, Philip A., primary, Kuroda, Mitzi I., primary, and French, Christopher A., primary

Published
2023
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16. Data from NSD3–NUT Fusion Oncoprotein in NUT Midline Carcinoma: Implications for a Novel Oncogenic Mechanism

Author

French, Christopher A., primary, Rahman, Shaila, primary, Walsh, Erica M., primary, Kühnle, Simone, primary, Grayson, Adlai R., primary, Lemieux, Madeleine E., primary, Grunfeld, Noam, primary, Rubin, Brian P., primary, Antonescu, Cristina R., primary, Zhang, Songlin, primary, Venkatramani, Rajkumar, primary, Dal Cin, Paola, primary, and Howley, Peter M., primary

Published
2023
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17. Supplementary Figure 4 from NSD3–NUT Fusion Oncoprotein in NUT Midline Carcinoma: Implications for a Novel Oncogenic Mechanism

Author

French, Christopher A., primary, Rahman, Shaila, primary, Walsh, Erica M., primary, Kühnle, Simone, primary, Grayson, Adlai R., primary, Lemieux, Madeleine E., primary, Grunfeld, Noam, primary, Rubin, Brian P., primary, Antonescu, Cristina R., primary, Zhang, Songlin, primary, Venkatramani, Rajkumar, primary, Dal Cin, Paola, primary, and Howley, Peter M., primary

Published
2023
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18. Supplementary Figure 3 from NSD3–NUT Fusion Oncoprotein in NUT Midline Carcinoma: Implications for a Novel Oncogenic Mechanism

Author

French, Christopher A., primary, Rahman, Shaila, primary, Walsh, Erica M., primary, Kühnle, Simone, primary, Grayson, Adlai R., primary, Lemieux, Madeleine E., primary, Grunfeld, Noam, primary, Rubin, Brian P., primary, Antonescu, Cristina R., primary, Zhang, Songlin, primary, Venkatramani, Rajkumar, primary, Dal Cin, Paola, primary, and Howley, Peter M., primary

Published
2023
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19. Supplementary Methods from Combined Targeting of the BRD4–NUT–p300 Axis in NUT Midline Carcinoma by Dual Selective Bromodomain Inhibitor, NEO2734

Author

Morrison-Smith, Chevaun D., primary, Knox, Tatiana M., primary, Filic, Ivona, primary, Soroko, Kara M., primary, Eschle, Benjamin K., primary, Wilkens, Margaret K., primary, Gokhale, Prafulla C., primary, Giles, Francis, primary, Griffin, Andrew, primary, Brown, Bill, primary, Shapiro, Geoffrey I., primary, Zucconi, Beth E., primary, Cole, Philip A., primary, Lemieux, Madeleine E., primary, and French, Christopher A., primary

Published
2023
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20. Supplemental Figures 1-9 from Combined Targeting of the BRD4–NUT–p300 Axis in NUT Midline Carcinoma by Dual Selective Bromodomain Inhibitor, NEO2734

Author

Morrison-Smith, Chevaun D., primary, Knox, Tatiana M., primary, Filic, Ivona, primary, Soroko, Kara M., primary, Eschle, Benjamin K., primary, Wilkens, Margaret K., primary, Gokhale, Prafulla C., primary, Giles, Francis, primary, Griffin, Andrew, primary, Brown, Bill, primary, Shapiro, Geoffrey I., primary, Zucconi, Beth E., primary, Cole, Philip A., primary, Lemieux, Madeleine E., primary, and French, Christopher A., primary

Published
2023
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21. Supplementary Figure 2 from NSD3–NUT Fusion Oncoprotein in NUT Midline Carcinoma: Implications for a Novel Oncogenic Mechanism

Author

French, Christopher A., primary, Rahman, Shaila, primary, Walsh, Erica M., primary, Kühnle, Simone, primary, Grayson, Adlai R., primary, Lemieux, Madeleine E., primary, Grunfeld, Noam, primary, Rubin, Brian P., primary, Antonescu, Cristina R., primary, Zhang, Songlin, primary, Venkatramani, Rajkumar, primary, Dal Cin, Paola, primary, and Howley, Peter M., primary

Published
2023
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22. Table S1 from Chemical Screen Identifies Diverse and Novel Histone Deacetylase Inhibitors as Repressors of NUT Function: Implications for NUT Carcinoma Pathogenesis and Treatment

Author

Shiota, Hitoshi, primary, Alekseyenko, Artyom A., primary, Wang, Zhipeng A., primary, Filic, Ivona, primary, Knox, Tatiana M., primary, Luong, Nhi M., primary, Huang, Yeying, primary, Scott, David A., primary, Jones, Kristen L., primary, Gokhale, Prafulla C., primary, Lemieux, Madeleine E., primary, Cole, Philip A., primary, Kuroda, Mitzi I., primary, and French, Christopher A., primary

Published
2023
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23. Supplementary Tables 1-3 from Combined Targeting of the BRD4–NUT–p300 Axis in NUT Midline Carcinoma by Dual Selective Bromodomain Inhibitor, NEO2734

Author

Morrison-Smith, Chevaun D., primary, Knox, Tatiana M., primary, Filic, Ivona, primary, Soroko, Kara M., primary, Eschle, Benjamin K., primary, Wilkens, Margaret K., primary, Gokhale, Prafulla C., primary, Giles, Francis, primary, Griffin, Andrew, primary, Brown, Bill, primary, Shapiro, Geoffrey I., primary, Zucconi, Beth E., primary, Cole, Philip A., primary, Lemieux, Madeleine E., primary, and French, Christopher A., primary

Published
2023
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24. Supplementary Figure 1 from NSD3–NUT Fusion Oncoprotein in NUT Midline Carcinoma: Implications for a Novel Oncogenic Mechanism

Author

French, Christopher A., primary, Rahman, Shaila, primary, Walsh, Erica M., primary, Kühnle, Simone, primary, Grayson, Adlai R., primary, Lemieux, Madeleine E., primary, Grunfeld, Noam, primary, Rubin, Brian P., primary, Antonescu, Cristina R., primary, Zhang, Songlin, primary, Venkatramani, Rajkumar, primary, Dal Cin, Paola, primary, and Howley, Peter M., primary

Published
2023
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25. Supplementary Data from Combined Targeting of the BRD4–NUT–p300 Axis in NUT Midline Carcinoma by Dual Selective Bromodomain Inhibitor, NEO2734

Author

Morrison-Smith, Chevaun D., primary, Knox, Tatiana M., primary, Filic, Ivona, primary, Soroko, Kara M., primary, Eschle, Benjamin K., primary, Wilkens, Margaret K., primary, Gokhale, Prafulla C., primary, Giles, Francis, primary, Griffin, Andrew, primary, Brown, Bill, primary, Shapiro, Geoffrey I., primary, Zucconi, Beth E., primary, Cole, Philip A., primary, Lemieux, Madeleine E., primary, and French, Christopher A., primary

Published
2023
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26. Supplementary Methods from Chemical Screen Identifies Diverse and Novel Histone Deacetylase Inhibitors as Repressors of NUT Function: Implications for NUT Carcinoma Pathogenesis and Treatment

Author

Shiota, Hitoshi, primary, Alekseyenko, Artyom A., primary, Wang, Zhipeng A., primary, Filic, Ivona, primary, Knox, Tatiana M., primary, Luong, Nhi M., primary, Huang, Yeying, primary, Scott, David A., primary, Jones, Kristen L., primary, Gokhale, Prafulla C., primary, Lemieux, Madeleine E., primary, Cole, Philip A., primary, Kuroda, Mitzi I., primary, and French, Christopher A., primary

Published
2023
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27. Supplementary Figure Legends from Chemical Screen Identifies Diverse and Novel Histone Deacetylase Inhibitors as Repressors of NUT Function: Implications for NUT Carcinoma Pathogenesis and Treatment

Author

Shiota, Hitoshi, primary, Alekseyenko, Artyom A., primary, Wang, Zhipeng A., primary, Filic, Ivona, primary, Knox, Tatiana M., primary, Luong, Nhi M., primary, Huang, Yeying, primary, Scott, David A., primary, Jones, Kristen L., primary, Gokhale, Prafulla C., primary, Lemieux, Madeleine E., primary, Cole, Philip A., primary, Kuroda, Mitzi I., primary, and French, Christopher A., primary

Published
2023
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28. Supplementary Figures 1-4 from Chemical Screen Identifies Diverse and Novel Histone Deacetylase Inhibitors as Repressors of NUT Function: Implications for NUT Carcinoma Pathogenesis and Treatment

Author

Shiota, Hitoshi, primary, Alekseyenko, Artyom A., primary, Wang, Zhipeng A., primary, Filic, Ivona, primary, Knox, Tatiana M., primary, Luong, Nhi M., primary, Huang, Yeying, primary, Scott, David A., primary, Jones, Kristen L., primary, Gokhale, Prafulla C., primary, Lemieux, Madeleine E., primary, Cole, Philip A., primary, Kuroda, Mitzi I., primary, and French, Christopher A., primary

Published
2023
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29. Macrophages directly contribute collagen to scar formation during zebrafish heart regeneration and mouse heart repair

Author

Simões, Filipa C., Cahill, Thomas J., Kenyon, Amy, Gavriouchkina, Daria, Vieira, Joaquim M., Sun, Xin, Pezzolla, Daniela, Ravaud, Christophe, Masmanian, Eva, Weinberger, Michael, Mayes, Sarah, Lemieux, Madeleine E., Barnette, Damien N., Gunadasa-Rohling, Mala, Williams, Ruth M., Greaves, David R., Trinh, Le A., Fraser, Scott E., Dallas, Sarah L., Choudhury, Robin P., Sauka-Spengler, Tatjana, and Riley, Paul R.

Published
2020
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30. Supplemental Table S1 from High-throughput Chemical Screening Identifies Focal Adhesion Kinase and Aurora Kinase B Inhibition as a Synergistic Treatment Combination in Ewing Sarcoma

Author

Wang, Sarah, primary, Hwang, Elizabeth E., primary, Guha, Rajarshi, primary, O'Neill, Allison F., primary, Melong, Nicole, primary, Veinotte, Chansey J., primary, Conway Saur, Amy, primary, Wuerthele, Kellsey, primary, Shen, Min, primary, McKnight, Crystal, primary, Alexe, Gabriela, primary, Lemieux, Madeleine E., primary, Wang, Amy, primary, Hughes, Emma, primary, Xu, Xin, primary, Boxer, Matthew B., primary, Hall, Matthew D., primary, Kung, Andrew, primary, Berman, Jason N., primary, Davis, Mindy I., primary, Stegmaier, Kimberly, primary, and Crompton, Brian D., primary

Published
2023
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31. Supplementary Data from High-throughput Chemical Screening Identifies Focal Adhesion Kinase and Aurora Kinase B Inhibition as a Synergistic Treatment Combination in Ewing Sarcoma

Author

Wang, Sarah, primary, Hwang, Elizabeth E., primary, Guha, Rajarshi, primary, O'Neill, Allison F., primary, Melong, Nicole, primary, Veinotte, Chansey J., primary, Conway Saur, Amy, primary, Wuerthele, Kellsey, primary, Shen, Min, primary, McKnight, Crystal, primary, Alexe, Gabriela, primary, Lemieux, Madeleine E., primary, Wang, Amy, primary, Hughes, Emma, primary, Xu, Xin, primary, Boxer, Matthew B., primary, Hall, Matthew D., primary, Kung, Andrew, primary, Berman, Jason N., primary, Davis, Mindy I., primary, Stegmaier, Kimberly, primary, and Crompton, Brian D., primary

Published
2023
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32. Data from Differentiation of NUT Midline Carcinoma by Epigenomic Reprogramming

Author

Schwartz, Brian E., primary, Hofer, Matthias D., primary, Lemieux, Madeleine E., primary, Bauer, Daniel E., primary, Cameron, Michael J., primary, West, Nathan H., primary, Agoston, Elin S., primary, Reynoird, Nicolas, primary, Khochbin, Saadi, primary, Ince, Tan A., primary, Christie, Amanda, primary, Janeway, Katherine A., primary, Vargas, Sara O., primary, Perez-Atayde, Antonio R., primary, Aster, Jon C., primary, Sallan, Stephen E., primary, Kung, Andrew L., primary, Bradner, James E., primary, and French, Christopher A., primary

Published
2023
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33. Supplementary Figures 1-2 from Differentiation of NUT Midline Carcinoma by Epigenomic Reprogramming

Author

Schwartz, Brian E., primary, Hofer, Matthias D., primary, Lemieux, Madeleine E., primary, Bauer, Daniel E., primary, Cameron, Michael J., primary, West, Nathan H., primary, Agoston, Elin S., primary, Reynoird, Nicolas, primary, Khochbin, Saadi, primary, Ince, Tan A., primary, Christie, Amanda, primary, Janeway, Katherine A., primary, Vargas, Sara O., primary, Perez-Atayde, Antonio R., primary, Aster, Jon C., primary, Sallan, Stephen E., primary, Kung, Andrew L., primary, Bradner, James E., primary, and French, Christopher A., primary

Published
2023
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34. Inhibition of Eicosanoid Degradation Mitigates Fibrosis of the Heart

Author

Rubino, Marcello, primary, Travers, Joshua G., additional, Headrick, Alaina L., additional, Enyart, Blake T., additional, Lemieux, Madeleine E., additional, Cavasin, Maria A., additional, Schwisow, Jessica A., additional, Hardy, Elizabeth J., additional, Kaltenbacher, Keenan J., additional, Felisbino, Marina B., additional, Jonas, Eric, additional, Ambardekar, Amrut V., additional, Bristow, Michael R., additional, Koch, Keith A., additional, and McKinsey, Timothy A., additional

Published
2023
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37. Correction: BPTF regulates growth of adult and pediatric high-grade glioma through the MYC pathway

Author

Green, Adam L., DeSisto, John, Flannery, Patrick, Lemma, Rakeb, Knox, Aaron, Lemieux, Madeleine, Sanford, Bridget, O’Rourke, Rebecca, Ramkissoon, Shakti, Jones, Kristen, Perry, Jennifer, Hui, Xu, Moroze, Erin, Balakrishnan, Ilango, O’Neill, Allison F., Dunn, Katherine, DeRyckere, Deborah, Danis, Etienne, Safadi, Aaron, Gilani, Ahmed, Hubbell-Engler, Benjamin, Nuss, Zachary, Levy, Jean M. Mulcahy, Serkova, Natalie, Venkataraman, Sujatha, Graham, Douglas K., Foreman, Nicholas, Ligon, Keith, Jones, Ken, Kung, Andrew L., and Vibhakar, Rajeev

Published
2020
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38. Mediator kinase inhibition further activates super-enhancer-associated genes in AML

Author

Pelish, Henry E., Liau, Brian B., Nitulescu, Ioana I., Tangpeerachaikul, Anupong, Poss, Zachary C., Silva, Diogo H. Da, Caruso, Brittany T., Arefolov, Alexander, Fadeyi, Olugbeminiyi, Christie, Amanda L., Du, Karrie, Banka, Deepti, Schneider, Elisabeth V., Jestel, Anja, Zou, Ge, Si, Chong, Ebmeier, Christopher C., Bronson, Roderick T., Krivtsov, Andrei V., Myers, Andrew G., Kohl, Nancy E., Kung, Andrew L., Armstrong, Scott A., Lemieux, Madeleine E., Taatjes, Dylan J., and Shair, Matthew D.

Subjects
Enzymes -- Regulation, Phosphotransferases -- Properties, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Super-enhancers (SEs), which are composed of large clusters of enhancers densely loaded with the Mediator complex, transcription factors and chromatin regulators, drive high expression of genes implicated in cell identity [...]

Published
2015

39. Monocytes transition to monocyte‐macrophages within the inflamed vasculature via CCR2 on monocytes and endothelial TNFR2

Author

Sathyanarayana Mysore, Vijayashree, primary, Tahir, Suhail, additional, Furuhashi, Kazuhiro, additional, Arora, Jatin, additional, Rosetti, Florencia, additional, Cullere, Xavier, additional, Yazbeck, Pascal, additional, Sekulic, Miroslav, additional, Lemieux, Madeleine E., additional, Raychaudhuri, Soumya, additional, Horwitz, Bruce, additional, and Mayadas, Tanya, additional

Published
2022
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40. Monocytes transition to macrophages within the inflamed vasculature via monocyte CCR2 and endothelial TNFR2

Author

Mysore, Vijayashree, primary, Tahir, Suhail, additional, Furuhashi, Kazuhiro, additional, Arora, Jatin, additional, Rosetti, Florencia, additional, Cullere, Xavier, additional, Yazbeck, Pascal, additional, Sekulic, Miroslav, additional, Lemieux, Madeleine E., additional, Raychaudhuri, Soumya, additional, Horwitz, Bruce H., additional, and Mayadas, Tanya N., additional

Published
2022
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46. Hyperglycemia Induces Trained Immunity in Macrophages and Their Precursors and Promotes Atherosclerosis

Author

Edgar, Laurienne, primary, Akbar, Naveed, additional, Braithwaite, Adam T., additional, Krausgruber, Thomas, additional, Gallart-Ayala, Héctor, additional, Bailey, Jade, additional, Corbin, Alastair L., additional, Khoyratty, Tariq E., additional, Chai, Joshua T., additional, Alkhalil, Mohammad, additional, Rendeiro, André F., additional, Ziberna, Klemen, additional, Arya, Ritu, additional, Cahill, Thomas J., additional, Bock, Christoph, additional, Laurencikiene, Jurga, additional, Crabtree, Mark J., additional, Lemieux, Madeleine E., additional, Riksen, Niels P., additional, Netea, Mihai G., additional, Wheelock, Craig E., additional, Channon, Keith M., additional, Rydén, Mikael, additional, Udalova, Irina A., additional, Carnicer, Ricardo, additional, and Choudhury, Robin P., additional

Published
2021
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47. Chemical Screen Identifies Diverse and Novel Histone Deacetylase Inhibitors as Repressors of NUT Function: Implications for NUT Carcinoma Pathogenesis and Treatment

Author

Shiota, Hitoshi, primary, Alekseyenko, Artyom A., additional, Wang, Zhipeng A., additional, Filic, Ivona, additional, Knox, Tatiana M., additional, Luong, Nhi M., additional, Huang, Yeying, additional, Scott, David A., additional, Jones, Kristen L., additional, Gokhale, Prafulla C., additional, Lemieux, Madeleine E., additional, Cole, Philip A., additional, Kuroda, Mitzi I., additional, and French, Christopher A., additional

Published
2021
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