Search

Your search keyword '"Allis, C. David"' showing total 1,176 results
Start Over Author "Allis, C. David"
1,176 results on '"Allis, C. David"'

1. Cancer-associated Histone H3 N-terminal arginine mutations disrupt PRC2 activity and impair differentiation

Author

Nacev, Benjamin A., Dabas, Yakshi, Paul, Matthew R., Pacheco, Christian, Mitchener, Michelle, Perez, Yekaterina, Fang, Yan, Soshnev, Alexey A., Barrows, Douglas, Carroll, Thomas, Socci, Nicholas D., St. Jean, Samantha C., Tiwari, Sagarika, Gruss, Michael J., Monette, Sebastien, Tap, William D., Garcia, Benjamin A., Muir, Tom, and Allis, C. David

Published
2024
Full Text
View/download PDF

3. MLL-AF4 cooperates with PAF1 and FACT to drive high-density enhancer interactions in leukemia

Author

Crump, Nicholas T., Smith, Alastair L., Godfrey, Laura, Dopico-Fernandez, Ana M., Denny, Nicholas, Harman, Joe R., Hamley, Joseph C., Jackson, Nicole E., Chahrour, Catherine, Riva, Simone, Rice, Siobhan, Kim, Jaehoon, Basrur, Venkatesha, Fermin, Damian, Elenitoba-Johnson, Kojo, Roeder, Robert G., Allis, C. David, Roberts, Irene, Roy, Anindita, Geng, Huimin, Davies, James O. J., and Milne, Thomas A.

Published
2023
Full Text
View/download PDF

4. Targeting integrated epigenetic and metabolic pathways in lethal childhood PFA ependymomas

Author

Panwalkar, Pooja, Tamrazi, Benita, Dang, Derek, Chung, Chan, Sweha, Stefan, Natarajan, Siva Kumar, Pun, Matthew, Bayliss, Jill, Ogrodzinski, Martin P, Pratt, Drew, Mullan, Brendan, Hawes, Debra, Yang, Fusheng, Lu, Chao, Sabari, Benjamin R, Achreja, Abhinav, Heon, Jin, Animasahun, Olamide, Cieslik, Marcin, Dunham, Christopher, Yip, Stephen, Hukin, Juliette, Phillips, Joanna J, Bornhorst, Miriam, Griesinger, Andrea M, Donson, Andrew M, Foreman, Nicholas K, Garton, Hugh JL, Heth, Jason, Muraszko, Karin, Nazarian, Javad, Koschmann, Carl, Jiang, Li, Filbin, Mariella G, Nagrath, Deepak, Kool, Marcel, Korshunov, Andrey, Pfister, Stefan M, Gilbertson, Richard J, Allis, C David, Chinnaiyan, Arul M, Lunt, Sophia Y, Blüml, Stefan, Judkins, Alexander R, and Venneti, Sriram

Subjects
Cancer, Biotechnology, Genetics, Rare Diseases, Orphan Drug, Neurosciences, Brain Disorders, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Animals, Child, Ependymoma, Epigenesis, Genetic, Epigenomics, Histones, Humans, Metabolic Networks and Pathways, Mice, Biological Sciences, Medical and Health Sciences
Abstract

Childhood posterior fossa group A ependymomas (PFAs) have limited treatment options and bear dismal prognoses compared to group B ependymomas (PFBs). PFAs overexpress the oncohistone-like protein EZHIP (enhancer of Zeste homologs inhibitory protein), causing global reduction of repressive histone H3 lysine 27 trimethylation (H3K27me3), similar to the oncohistone H3K27M. Integrated metabolic analyses in patient-derived cells and tumors, single-cell RNA sequencing of tumors, and noninvasive metabolic imaging in patients demonstrated enhanced glycolysis and tricarboxylic acid (TCA) cycle metabolism in PFAs. Furthermore, high glycolytic gene expression in PFAs was associated with a poor outcome. PFAs demonstrated high EZHIP expression associated with poor prognosis and elevated activating mark histone H3 lysine 27 acetylation (H3K27ac). Genomic H3K27ac was enriched in PFAs at key glycolytic and TCA cycle–related genes including hexokinase-2 and pyruvate dehydrogenase. Similarly, mouse neuronal stem cells (NSCs) expressing wild-type EZHIP (EZHIP-WT) versus catalytically attenuated EZHIP-M406K demonstrated H3K27ac enrichment at hexokinase-2 and pyruvate dehydrogenase, accompanied by enhanced glycolysis and TCA cycle metabolism. AMPKα-2, a key component of the metabolic regulator AMP-activated protein kinase (AMPK), also showed H3K27ac enrichment in PFAs and EZHIP-WT NSCs. The AMPK activator metformin lowered EZHIP protein concentrations, increased H3K27me3, suppressed TCA cycle metabolism, and showed therapeutic efficacy in vitro and in vivo in patient-derived PFA xenografts in mice. Our data indicate that PFAs and EZHIP-WT–expressing NSCs are characterized by enhanced glycolysis and TCA cycle metabolism. Repurposing the antidiabetic drug metformin lowered pathogenic EZHIP, increased H3K27me3, and suppressed tumor growth, suggesting that targeting integrated metabolic/epigenetic pathways is a potential therapeutic strategy for treating childhood ependymomas.

Published
2021

7. Lead Optimization of Small Molecule ENL YEATS Inhibitors to Enable In Vivo Studies: Discovery of TDI-11055

Author

Michino, Mayako, primary, Khan, Tanweer A., additional, Miller, Michael W., additional, Fukase, Yoshiyuki, additional, Vendome, Jeremie, additional, Adura, Carolina, additional, Glickman, J. Fraser, additional, Liu, Yiman, additional, Wan, Liling, additional, Allis, C. David, additional, Stamford, Andrew W., additional, Meinke, Peter T., additional, Renzetti, Louis M., additional, Kargman, Stacia, additional, Liverton, Nigel J., additional, and Huggins, David J., additional

Published
2024
Full Text
View/download PDF

13. Lowered H3K27me3 and DNA hypomethylation define poorly prognostic pediatric posterior fossa ependymomas

Author

Bayliss, Jill, Mukherjee, Piali, Lu, Chao, Jain, Siddhant U, Chung, Chan, Martinez, Daniel, Sabari, Benjamin, Margol, Ashley S, Panwalkar, Pooja, Parolia, Abhijit, Pekmezci, Melike, McEachin, Richard C, Cieslik, Marcin, Tamrazi, Benita, Garcia, Benjamin A, La Rocca, Gaspare, Santi, Mariarita, Lewis, Peter W, Hawkins, Cynthia, Melnick, Ari, Allis, C David, Thompson, Craig B, Chinnaiyan, Arul M, Judkins, Alexander R, and Venneti, Sriram

Subjects
Medical Biotechnology, Biomedical and Clinical Sciences, Brain Disorders, Pediatric, Neurosciences, Human Genome, Rare Diseases, Cancer, Pediatric Cancer, Brain Cancer, Genetics, Brain Neoplasms, Central Nervous System, Child, CpG Islands, DNA Methylation, Ependymoma, Epigenesis, Genetic, Gene Expression Profiling, Genome, Human, Histones, Humans, Mutation, Prognosis, Treatment Outcome, Biological Sciences, Medical and Health Sciences, Medical biotechnology, Biomedical engineering
Abstract

Childhood posterior fossa (PF) ependymomas cause substantial morbidity and mortality. These tumors lack recurrent genetic mutations, but a subset of these ependymomas exhibits CpG island (CpGi) hypermethylation [PF group A (PFA)], implicating epigenetic alterations in their pathogenesis. Further, histological grade does not reliably predict prognosis, highlighting the importance of developing more robust prognostic markers. We discovered global H3K27me3 reduction in a subset of these tumors (PF-ve ependymomas) analogous to H3K27M mutant gliomas. PF-ve tumors exhibited many clinical and biological similarities with PFA ependymomas. Genomic H3K27me3 distribution showed an inverse relationship with CpGi methylation, suggesting that CpGi hypermethylation drives low H3K27me3 in PF-ve ependymomas. Despite CpGi hypermethylation and global H3K27me3 reduction, these tumors showed DNA hypomethylation in the rest of the genome and exhibited increased H3K27me3 genomic enrichment at limited genomic loci similar to H3K27M mutant gliomas. Combined integrative analysis of PF-ve ependymomas with H3K27M gliomas uncovered common epigenetic deregulation of select factors that control radial glial biology, and PF radial glia in early human development exhibited reduced H3K27me3. Finally, H3K27me3 immunostaining served as a biomarker of poor prognosis and delineated radiologically invasive tumors, suggesting that reduced H3K27me3 may be a prognostic indicator in PF ependymomas.

Published
2016

14. Histone H1 loss drives lymphoma by disrupting 3D chromatin architecture

Author

Yusufova, Nevin, Kloetgen, Andreas, Teater, Matt, Osunsade, Adewola, Camarillo, Jeannie M., Chin, Christopher R., Doane, Ashley S., Venters, Bryan J., Portillo-Ledesma, Stephanie, Conway, Joseph, Phillip, Jude M., Elemento, Olivier, Scott, David W., Béguelin, Wendy, Licht, Jonathan D., Kelleher, Neil L., Staudt, Louis M., Skoultchi, Arthur I., Keogh, Michael-Christopher, Apostolou, Effie, Mason, Christopher E., Imielinski, Marcin, Schlick, Tamar, David, Yael, Tsirigos, Aristotelis, Allis, C. David, Soshnev, Alexey A., Cesarman, Ethel, and Melnick, Ari M.

Published
2021
Full Text
View/download PDF

15. Chromatin Kinases Act on Transcription Factors and Histone Tails in Regulation of Inducible Transcription

Author

Josefowicz, Steven Z, Shimada, Miho, Armache, Anja, Li, Charles H, Miller, Rand M, Lin, Shu, Yang, Aerin, Dill, Brian D, Molina, Henrik, Park, Hee-Sung, Garcia, Benjamin A, Taunton, Jack, Roeder, Robert G, and Allis, C David

Subjects
Biochemistry and Cell Biology, Biological Sciences, Genetics, Aetiology, 1.1 Normal biological development and functioning, Underpinning research, 2.1 Biological and endogenous factors, Bacterial Proteins, Cell Cycle Proteins, Cell Line, Tumor, Chromatin, Epithelial Cells, Feedback, Physiological, HeLa Cells, Histones, Humans, Kinetics, Luminescent Proteins, Mitosis, Models, Statistical, Molecular Imaging, Recombinant Fusion Proteins, Time Factors, Transcription Factors, Transcription, Genetic, Hela Cells, H3S28ph, chromatin, epigenetics, histone phosphorylation, inflammation, macrophage, mitogen- and stress-activated protein kinase, p300, transcription, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

The inflammatory response requires coordinated activation of both transcription factors and chromatin to induce transcription for defense against pathogens and environmental insults. We sought to elucidate the connections between inflammatory signaling pathways and chromatin through genomic footprinting of kinase activity and unbiased identification of prominent histone phosphorylation events. We identified H3 serine 28 phosphorylation (H3S28ph) as the principal stimulation-dependent histone modification and observed its enrichment at induced genes in mouse macrophages stimulated with bacterial lipopolysaccharide. Using pharmacological and genetic approaches, we identified mitogen- and stress-activated protein kinases (MSKs) as primary mediators of H3S28ph in macrophages. Cell-free transcription assays demonstrated that H3S28ph directly promotes p300/CBP-dependent transcription. Further, MSKs can activate both signal-responsive transcription factors and the chromatin template with additive effects on transcription. Specific inhibition of MSKs in macrophages selectively reduced transcription of stimulation-induced genes. Our results suggest that MSKs incorporate upstream signaling inputs and control multiple downstream regulators of inducible transcription.

Published
2016

17. Target identification reveals lanosterol synthase as a vulnerability in glioma

Author

Phillips, Richard E., Yang, Yanhong, Smith, Ryan C., Thompson, Bonne M., Yamasaki, Tomoko, Soto-Feliciano, Yadira M., Funato, Kosuke, Liang, Yupu, Garcia-Bermudez, Javier, Wang, Xiaoshi, Garcia, Benjamin A., Yamasaki, Kazuhiko, McDonald, Jeffrey G., Birsoy, Kivanç, Tabar, Viviane, and Allis, C. David

Published
2019

18. The epigenomics of sarcoma

Author

Nacev, Benjamin A., Jones, Kevin B., Intlekofer, Andrew M., Yu, Jamie S. E., Allis, C. David, Tap, William D., Ladanyi, Marc, and Nielsen, Torsten O.

Published
2020
Full Text
View/download PDF

19. Histone H3.3 phosphorylation amplifies stimulation-induced transcription

Author

Armache, Anja, Yang, Shuang, Martínez de Paz, Alexia, Robbins, Lexi E., Durmaz, Ceyda, Cheong, Jin Q., Ravishankar, Arjun, Daman, Andrew W., Ahimovic, Dughan J., Klevorn, Thaís, Yue, Yuan, Arslan, Tanja, Lin, Shu, Panchenko, Tanya, Hrit, Joel, Wang, Miao, Thudium, Samuel, Garcia, Benjamin A., Korb, Erica, Armache, Karim-Jean, Rothbart, Scott B., Hake, Sandra B., Allis, C. David, Li, Haitao, and Josefowicz, Steven Z.

Published
2020
Full Text
View/download PDF

21. Altered chromatin occupancy of patient-associated H4 mutants misregulate neuronal differentiation

Author

Feng, Lijuan, primary, Barrows, Douglas, additional, Zhong, Liangwen, additional, Matlik, Kart, additional, Porter, Elizabeth G., additional, Djomo, Annaelle M., additional, Yau, Iris, additional, Soshnev, Alexey A., additional, Carroll, Thomas S., additional, Wen, Duancheng, additional, Hatten, Mary E., additional, Garcia, Benjamin A., additional, and Allis, C. David, additional

Published
2023
Full Text
View/download PDF

22. The histone mark H3K36me2 recruits DNMT3A and shapes the intergenic DNA methylation landscape

Author

Weinberg, Daniel N., Papillon-Cavanagh, Simon, Chen, Haifen, Yue, Yuan, Chen, Xiao, Rajagopalan, Kartik N., Horth, Cynthia, McGuire, John T., Xu, Xinjing, Nikbakht, Hamid, Lemiesz, Agata E., Marchione, Dylan M., Marunde, Matthew R., Meiners, Matthew J., Cheek, Marcus A., Keogh, Michael-Christopher, Bareke, Eric, Djedid, Anissa, Harutyunyan, Ashot S., Jabado, Nada, Garcia, Benjamin A., Li, Haitao, Allis, C. David, Majewski, Jacek, and Lu, Chao

Published
2019
Full Text
View/download PDF

31. MLL3 regulates the CDKN2A tumor suppressor locus in liver cancer

Author

Zhu, Changyu, primary, Soto-Feliciano, Yadira M, additional, Morris, John P, additional, Huang, Chun-Hao, additional, Koche, Richard P, additional, Ho, Yu-jui, additional, Banito, Ana, additional, Chen, Chun-Wei (David), additional, Shroff, Aditya, additional, Tian, Sha, additional, Livshits, Geulah, additional, Chen, Chi-Chao, additional, Fennell, Myles, additional, Armstrong, Scott A, additional, Allis, C David, additional, Tschaharganeh, Darjus F, additional, and Lowe, Scott W, additional

Published
2023
Full Text
View/download PDF

47. Supplementary Table 3 from A Molecular Switch between Mammalian MLL Complexes Dictates Response to Menin–MLL Inhibition

Author

Soto-Feliciano, Yadira M., primary, Sánchez-Rivera, Francisco J., primary, Perner, Florian, primary, Barrows, Douglas W., primary, Kastenhuber, Edward R., primary, Ho, Yu-Jui, primary, Carroll, Thomas, primary, Xiong, Yijun, primary, Anand, Disha, primary, Soshnev, Alexey A., primary, Gates, Leah, primary, Beytagh, Mary Clare, primary, Cheon, David, primary, Gu, Shengqing, primary, Liu, X. Shirley, primary, Krivtsov, Andrei V., primary, Meneses, Maximiliano, primary, de Stanchina, Elisa, primary, Stone, Richard M., primary, Armstrong, Scott A., primary, Lowe, Scott W., primary, and Allis, C. David, primary

Published
2023
Full Text
View/download PDF

48. Data from A Molecular Switch between Mammalian MLL Complexes Dictates Response to Menin–MLL Inhibition

Author

Soto-Feliciano, Yadira M., primary, Sánchez-Rivera, Francisco J., primary, Perner, Florian, primary, Barrows, Douglas W., primary, Kastenhuber, Edward R., primary, Ho, Yu-Jui, primary, Carroll, Thomas, primary, Xiong, Yijun, primary, Anand, Disha, primary, Soshnev, Alexey A., primary, Gates, Leah, primary, Beytagh, Mary Clare, primary, Cheon, David, primary, Gu, Shengqing, primary, Liu, X. Shirley, primary, Krivtsov, Andrei V., primary, Meneses, Maximiliano, primary, de Stanchina, Elisa, primary, Stone, Richard M., primary, Armstrong, Scott A., primary, Lowe, Scott W., primary, and Allis, C. David, primary

Published
2023
Full Text
View/download PDF

49. Supplementary Table 2 from A Molecular Switch between Mammalian MLL Complexes Dictates Response to Menin–MLL Inhibition

Author

Soto-Feliciano, Yadira M., primary, Sánchez-Rivera, Francisco J., primary, Perner, Florian, primary, Barrows, Douglas W., primary, Kastenhuber, Edward R., primary, Ho, Yu-Jui, primary, Carroll, Thomas, primary, Xiong, Yijun, primary, Anand, Disha, primary, Soshnev, Alexey A., primary, Gates, Leah, primary, Beytagh, Mary Clare, primary, Cheon, David, primary, Gu, Shengqing, primary, Liu, X. Shirley, primary, Krivtsov, Andrei V., primary, Meneses, Maximiliano, primary, de Stanchina, Elisa, primary, Stone, Richard M., primary, Armstrong, Scott A., primary, Lowe, Scott W., primary, and Allis, C. David, primary

Published
2023
Full Text
View/download PDF

50. Supplementary Table 4 from A Molecular Switch between Mammalian MLL Complexes Dictates Response to Menin–MLL Inhibition

Author

Soto-Feliciano, Yadira M., primary, Sánchez-Rivera, Francisco J., primary, Perner, Florian, primary, Barrows, Douglas W., primary, Kastenhuber, Edward R., primary, Ho, Yu-Jui, primary, Carroll, Thomas, primary, Xiong, Yijun, primary, Anand, Disha, primary, Soshnev, Alexey A., primary, Gates, Leah, primary, Beytagh, Mary Clare, primary, Cheon, David, primary, Gu, Shengqing, primary, Liu, X. Shirley, primary, Krivtsov, Andrei V., primary, Meneses, Maximiliano, primary, de Stanchina, Elisa, primary, Stone, Richard M., primary, Armstrong, Scott A., primary, Lowe, Scott W., primary, and Allis, C. David, primary

Published
2023
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results