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201. Leveraging Gas-Phase Fragmentation Pathways for Improved Identification and Selective Detection of Targets Modified by Covalent Probes

Author

Ficarro, Scott B., primary, Browne, Christopher M., additional, Card, Joseph D., additional, Alexander, William M., additional, Zhang, Tinghu, additional, Park, Eunyoung, additional, McNally, Randall, additional, Dhe-Paganon, Sirano, additional, Seo, Hyuk-Soo, additional, Lamberto, Ilaria, additional, Eck, Michael J., additional, Buhrlage, Sara J., additional, Gray, Nathanael S., additional, and Marto, Jarrod A., additional

Published
2016
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202. Proteomic Landscape of Tissue-Specific Cyclin E Functions in Vivo

Author

Odajima, Junko, primary, Saini, Siddharth, additional, Jung, Piotr, additional, Ndassa-Colday, Yasmine, additional, Ficaro, Scott, additional, Geng, Yan, additional, Marco, Eugenio, additional, Michowski, Wojciech, additional, Wang, Yaoyu E., additional, DeCaprio, James A., additional, Litovchick, Larisa, additional, Marto, Jarrod, additional, and Sicinski, Piotr, additional

Published
2016
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203. Differential contribution of the mitochondrial translation pathway to the survival of diffuse large B-cell lymphoma subsets

Author

Norberg, Erik, primary, Lako, Ana, additional, Chen, Pei-Hsuan, additional, Stanley, Illana A, additional, Zhou, Feng, additional, Ficarro, Scott B, additional, Chapuy, Bjoern, additional, Chen, Linfeng, additional, Rodig, Scott, additional, Shin, Donghyuk, additional, Choi, Dong Wook, additional, Lee, Sangho, additional, Shipp, Margaret A, additional, Marto, Jarrod A, additional, and Danial, Nika N, additional

Published
2016
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205. Covalent targeting of remote cysteine residues to develop CDK12 and CDK13 inhibitors

Author

Zhang, Tinghu, primary, Kwiatkowski, Nicholas, additional, Olson, Calla M, additional, Dixon-Clarke, Sarah E, additional, Abraham, Brian J, additional, Greifenberg, Ann K, additional, Ficarro, Scott B, additional, Elkins, Jonathan M, additional, Liang, Yanke, additional, Hannett, Nancy M, additional, Manz, Theresa, additional, Hao, Mingfeng, additional, Bartkowiak, Bartlomiej, additional, Greenleaf, Arno L, additional, Marto, Jarrod A, additional, Geyer, Matthias, additional, Bullock, Alex N, additional, Young, Richard A, additional, and Gray, Nathanael S, additional

Published
2016
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207. LIN28 Regulates Stem Cell Metabolism and Conversion to Primed Pluripotency

Author

Zhang, Jin, primary, Ratanasirintrawoot, Sutheera, additional, Chandrasekaran, Sriram, additional, Wu, Zhaoting, additional, Ficarro, Scott B., additional, Yu, Chunxiao, additional, Ross, Christian A., additional, Cacchiarelli, Davide, additional, Xia, Qing, additional, Seligson, Marc, additional, Shinoda, Gen, additional, Xie, Wen, additional, Cahan, Patrick, additional, Wang, Longfei, additional, Ng, Shyh-Chang, additional, Tintara, Supisara, additional, Trapnell, Cole, additional, Onder, Tamer, additional, Loh, Yuin-Han, additional, Mikkelsen, Tarjei, additional, Sliz, Piotr, additional, Teitell, Michael A., additional, Asara, John M., additional, Marto, Jarrod A., additional, Li, Hu, additional, Collins, James J., additional, and Daley, George Q., additional

Published
2016
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211. TRIP13 regulates DNA repair pathway choice through REV7 conformational change

Author

Clairmont, Connor S., Sarangi, Prabha, Ponnienselvan, Karthikeyan, Galli, Lucas D., Csete, Isabelle, Moreau, Lisa, Adelmant, Guillaume, Chowdhury, Dipanjan, Marto, Jarrod A., and D’Andrea, Alan D.

Abstract

DNA double-strand breaks (DSBs) are repaired through homology-directed repair (HDR) or non-homologous end joining (NHEJ). BRCA1/2-deficient cancer cells cannot perform HDR, conferring sensitivity to poly(ADP-ribose) polymerase inhibitors (PARPi). However, concomitant loss of the pro-NHEJ factors 53BP1, RIF1, REV7–Shieldin (SHLD1–3) or CST–DNA polymerase alpha (Pol-α) in BRCA1-deficient cells restores HDR and PARPi resistance. Here, we identify the TRIP13 ATPase as a negative regulator of REV7. We show that REV7 exists in active ‘closed’ and inactive ‘open’ conformations, and TRIP13 catalyses the inactivating conformational change, thereby dissociating REV7–Shieldin to promote HDR. TRIP13 similarly disassembles the REV7–REV3 translesion synthesis (TLS) complex, a component of the Fanconi anaemia pathway, inhibiting error-prone replicative lesion bypass and interstrand crosslink repair. Importantly, TRIP13 overexpression is common in BRCA1-deficient cancers, confers PARPi resistance and correlates with poor prognosis. Thus, TRIP13 emerges as an important regulator of DNA repair pathway choice—promoting HDR, while suppressing NHEJ and TLS.

Published
2020
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213. Author Correction: The Cyclophilin A–CD147 complex promotes the proliferation and homing of multiple myeloma cells

Author

Zhu, Di, Wang, Zhongqiu, Zhao, Jian-Jun, Calimeri, Teresa, Meng, Jiang, Hideshima, Teru, Fulciniti, Mariateresa, Kang, Yue, Ficarro, Scott B., Tai, Yu-Tzu, Hunter, Zachary, McMilin, Douglas, Tong, Haoxuan, Mitsiades, Constantine S., Wu, Catherine J., Treon, Steven P., Dorfman, David M., Pinkus, Geraldine, Munshi, Nikhil C., Tassone, Pierfrancesco, Marto, Jarrod A., Anderson, Kenneth C., and Carrasco, Ruben D.

Published
2024
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214. Phosphoproteomic analysis reveals that PP4 dephosphorylates KAP-1 impacting the DNA damage response

Author

Lee, Dong-Hyun, Goodarzi, Aaron A, Adelmant, Guillaume O, Pan, Yunfeng, Jeggo, Penelope A, Marto, Jarrod A, and Chowdhury, Dipanjan

Subjects
G2 Phase, DNA, Tripartite Motif-Containing Protein 28, Models, Biological, Article, Repressor Proteins, Radiation, Ionizing, Phosphoprotein Phosphatases, Humans, Phosphorylation, Protein Processing, Post-Translational, Cell Division, DNA Damage, HeLa Cells
Abstract

Protein phosphatase PP4C has been implicated in the DNA damage response (DDR), but its substrates in DDR remain largely unknown. We devised a novel proteomic strategy for systematic identification of proteins dephosphorylated by PP4C and identified KRAB-domain-associated protein 1 (KAP-1) as a substrate. Ionizing radiation leads to phosphorylation of KAP-1 at S824 (via ATM) and at S473 (via CHK2). A PP4C/R3β complex interacts with KAP-1 and silencing this complex leads to persistence of phospho-S824 and phospho-S473. We identify a new role for KAP-1 in DDR by showing that phosphorylation of S473 impacts the G2/M checkpoint. Depletion of PP4R3β or expression of the phosphomimetic KAP-1 S473 mutant (S473D) leads to a prolonged G2/M checkpoint. Phosphorylation of S824 is necessary for repair of heterochromatic DNA lesions and similar to cells expressing phosphomimetic KAP-1 S824 mutant (S824D), or PP4R3β-silenced cells, display prolonged relaxation of chromatin with release of chromatin remodelling protein CHD3. Our results define a new role for PP4-mediated dephosphorylation in the DDR, including the regulation of a previously undescribed function of KAP-1 in checkpoint response.

Published
2011

215. An Online Nanoflow RP-SAX-RP LC-MS/MS Platform for Efficient and In-depth Proteome Sequence Analysis of Complex Organisms

Author

Zhou, Feng, Sikorski, Timothy W., Ficarro, Scott B., Webber, James T., and Marto, Jarrod A.

Subjects
Chromatography, Reverse-Phase, Saccharomyces cerevisiae Proteins, Proteome, Tandem Mass Spectrometry, Escherichia coli Proteins, Escherichia coli, Nanotechnology, Trypsin, Saccharomyces cerevisiae, Chromatography, Ion Exchange, Peptides, Article
Abstract

The dynamic range of protein expression in complex organisms coupled with the stochastic nature of discovery-driven tandem mass spectrometry (MS/MS) analysis continues to impede comprehensive sequence analysis and often provides only limited information for low-abundance proteins. High-performance fractionation of proteins or peptides prior to mass spectrometry analysis can mitigate these effects, though achieving an optimal combination of automation, reproducibility, separation peak capacity, and sample yield remains a significant challenge. Here we demonstrate an automated nanoflow 3-D liquid chromatography (LC)-MS/MS platform based on high-pH reversed phase (RP), strong anion exchange (SAX), and low-pH reversed phase (RP) separation stages for analysis of complex proteomes. We observed that RP-SAX-RP outperformed RP-RP for analysis of tryptic peptides derived from Escherichia coli and enabled identification of proteins present at a level of 50 copies per cell in Saccharomyces cerevisiae, corresponding to an estimated detection limit of 500 amol, from 40 μg of total lysate on a low-resolution 3-D ion trap mass spectrometer. A similar study performed on a LTQ-Orbitrap yielded over 4000 unique proteins from 5 μg of total yeast lysate analyzed in a single, 101 fraction RP-SAX-RP LC-MS/MS acquisition, providing an estimated detection limit of 65 amol for proteins expressed at 50 copies per cell.

Published
2011

217. Targeting transcription regulation in cancer with a covalent CDK7 inhibitor

Author

Massachusetts Institute of Technology. Department of Biology, Whitehead Institute for Biomedical Research, Reddy, Jessica, Young, Richard A., Kwiatkowski, Nicholas P., Zhang, Tinghu, Rahl, Peter B., Abraham, Brian J., Ficarro, Scott B., Dastur, Anahita, Amzallag, Arnaud, Ramaswamy, Sridhar, Tesar, Bethany, Jenkins, Catherine E., Hannett, Nancy M., McMillin, Douglas, Sanda, Takaomi, Sim, Taebo, Kim, Nam Doo, Look, A. Thomas, Mitsiades, Constantine S., Weng, Andrew P., Brown, Jennifer R., Benes, Cyril H., Marto, Jarrod A., Gray, Nathanael S., Massachusetts Institute of Technology. Department of Biology, Whitehead Institute for Biomedical Research, Reddy, Jessica, Young, Richard A., Kwiatkowski, Nicholas P., Zhang, Tinghu, Rahl, Peter B., Abraham, Brian J., Ficarro, Scott B., Dastur, Anahita, Amzallag, Arnaud, Ramaswamy, Sridhar, Tesar, Bethany, Jenkins, Catherine E., Hannett, Nancy M., McMillin, Douglas, Sanda, Takaomi, Sim, Taebo, Kim, Nam Doo, Look, A. Thomas, Mitsiades, Constantine S., Weng, Andrew P., Brown, Jennifer R., Benes, Cyril H., Marto, Jarrod A., and Gray, Nathanael S.

Abstract

Tumour oncogenes include transcription factors that co-opt the general transcriptional machinery to sustain the oncogenic state, but direct pharmacological inhibition of transcription factors has so far proven difficult. However, the transcriptional machinery contains various enzymatic cofactors that can be targeted for the development of new therapeutic candidates, including cyclin-dependent kinases (CDKs). Here we present the discovery and characterization of a covalent CDK7 inhibitor, THZ1, which has the unprecedented ability to target a remote cysteine residue located outside of the canonical kinase domain, providing an unanticipated means of achieving selectivity for CDK7. Cancer cell-line profiling indicates that a subset of cancer cell lines, including human T-cell acute lymphoblastic leukaemia (T-ALL), have exceptional sensitivity to THZ1. Genome-wide analysis in Jurkat T-ALL cells shows that THZ1 disproportionally affects transcription of RUNX1 and suggests that sensitivity to THZ1 may be due to vulnerability conferred by the RUNX1 super-enhancer and the key role of RUNX1 in the core transcriptional regulatory circuitry of these tumour cells. Pharmacological modulation of CDK7 kinase activity may thus provide an approach to identify and treat tumour types that are dependent on transcription for maintenance of the oncogenic state., National Institutes of Health (U.S.) (Grant HG002668), National Institutes of Health (U.S.) (Grant CA109901)

Published
2015

218. Genomic and Proteomic Analysis of Primary Chemoresistance and Induction Failure in Acute Myeloid Leukemia

Author

Brown, Fiona, primary, Still, Eric, additional, Cifani, Paolo, additional, Ficarro, Scott, additional, Pouliot, Gayle, additional, Drill, Esther, additional, Gonen, Mithat, additional, He, Jie, additional, Balasubramanian, Sohail, additional, Zhong, Shan, additional, Pavlick, Dean, additional, Yilmazel, Bahar, additional, Krivtsov, Andrei V., additional, Alonzo, Todd A., additional, Meshinchi, Soheil, additional, Kornblau, Steven M., additional, Stone, Richard M., additional, Marcucci, Guido, additional, Byrd, John C., additional, Levine, Ross L., additional, Armstrong, Scott A., additional, Gray, Nathanael, additional, Marto, Jarrod, additional, and Kentsis, Alex, additional

Published
2015
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221. Development of Selective Covalent Janus Kinase 3 Inhibitors

Author

Tan, Li, primary, Akahane, Koshi, additional, McNally, Randall, additional, Reyskens, Kathleen M. S. E., additional, Ficarro, Scott B., additional, Liu, Suhu, additional, Herter-Sprie, Grit S., additional, Koyama, Shohei, additional, Pattison, Michael J., additional, Labella, Katherine, additional, Johannessen, Liv, additional, Akbay, Esra A., additional, Wong, Kwok-Kin, additional, Frank, David A., additional, Marto, Jarrod A., additional, Look, Thomas A., additional, Arthur, J. Simon C., additional, Eck, Michael J., additional, and Gray, Nathanael S., additional

Published
2015
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222. Structure and mechanism of activity-based inhibition of the EGF receptor by Mig6

Author

Park, Eunyoung, primary, Kim, Nayoung, additional, Ficarro, Scott B, additional, Zhang, Yi, additional, Lee, Byung Il, additional, Cho, Ahye, additional, Kim, Kihong, additional, Park, Angela K J, additional, Park, Woong-Yang, additional, Murray, Bradley, additional, Meyerson, Matthew, additional, Beroukhim, Rameen, additional, Marto, Jarrod A, additional, Cho, Jeonghee, additional, and Eck, Michael J, additional

Published
2015
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226. Pathway Palette: a rich internet application for peptide-, protein- and network-oriented analysis of mass spectrometry data

Author

Askenazi, Manor, Li, Shaojuan, Singh, Saurav, and Marto, Jarrod A.

Subjects
Proteomics, Internet, ComputingMethodologies_PATTERNRECOGNITION, Molecular Sequence Data, Proteins, Amino Acid Sequence, Peptides, Article, Mass Spectrometry
Abstract

Recent improvements in proteomic technologies have collectively yielded data sets that far exceed the capabilities of typical low-throughput interpretation strategies. Unfortunately, tools designed to leverage the "peptide-centric" content of MS-based proteomics lag the current rate of data production. Here, we describe Pathway Palette (http://blaispathways.dfci.harvard.edu), a freely accessible internet application that enables researchers to easily transition from peptides to biological pathways, while simultaneously retaining the qualitative and quantitative aspects of the underlying MS data.

Published
2010

227. The Cyclophilin A–CD147 complex promotes the proliferation and homing of multiple myeloma cells

Author

Zhu, Di, primary, Wang, Zhongqiu, additional, Zhao, Jian-Jun, additional, Calimeri, Teresa, additional, Meng, Jiang, additional, Hideshima, Teru, additional, Fulciniti, Mariateresa, additional, Kang, Yue, additional, Ficarro, Scott B, additional, Tai, Yu-Tzu, additional, Hunter, Zachary, additional, McMilin, Douglas, additional, Tong, Haoxuan, additional, Mitsiades, Constantine S, additional, Wu, Catherine J, additional, Treon, Steven P, additional, Dorfman, David M, additional, Pinkus, Geraldine, additional, Munshi, Nikhil C, additional, Tassone, Pierfrancesco, additional, Marto, Jarrod A, additional, Anderson, Kenneth C, additional, and Carrasco, Ruben D, additional

Published
2015
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228. Hepatic Dysfunction Caused by Consumption of a High-Fat Diet.

Author

Soltis, Anthony R., Kennedy, Norman J., Xiaofeng Xin, Feng Zhou, Ficarro, Scott B., Yoon Sing Yap, Matthews, Bryan J., Lauffenburger, Douglas A., White, Forest M., Marto, Jarrod A., Davis, Roger J., and Fraenkel, Ernest

Abstract

Obesity is a major human health crisis that promotes insulin resistance and, ultimately, type 2 diabetes. The molecular mechanisms that mediate this response occur across many highly complex biological regulatory levels that are incompletely understood. Here, we present a comprehensive molecular systems biology study of hepatic responses to highfat feeding in mice. We interrogated diet-induced epigenomic, transcriptomic, proteomic, and metabolomic alterations using high-throughput omic methods and used a network modeling approach to integrate these diverse molecular signals. Our model indicated that disruption of hepatic architecture and enhanced hepatocyte apoptosis are among the numerous biological processes that contribute to early liver dysfunction and low-grade inflammation during the development of dietinduced metabolic syndrome. We validated these model findings with additional experiments on mouse liver sections. In total, we present an integrative systems biology study of diet-induced hepatic insulin resistance that uncovered molecular features promoting the development and maintenance of metabolic disease. [ABSTRACT FROM AUTHOR]

Published
2017
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230. A Sequentially Priming Phosphorylation Cascade Activates the Gliomagenic Transcription Factor Olig2.

Author

Jing Zhou, An-Chi Tien, Alberta, John A., Ficarro, Scott B., Griveau, Amelie, Yu Sun, Deshpande, Janhavee S., Card, Joseph D., Morgan-Smith, Meghan, Michowski, Wojciech, Hashizume, Rintaro, James, C. David, Ligon, Keith L., Snider, William D., Sicinski, Peter, Marto, Jarrod A., Rowitch, David H., and Stiles, Charles D.

Abstract

During development of the vertebrate CNS, the basic helix-loop-helix (bHLH) transcription factor Olig2 sustains replication competence of progenitor cells that give rise to neurons and oligodendrocytes. A pathological counterpart of this developmental function is seen in human glioma, wherein Olig2 is required for maintenance of stem-like cells that drive tumor growth. The mitogenic/gliomagenic functions of Olig2 are regulated by phosphorylation of a triple serine motif (S10, S13, and S14) in the amino terminus. Here, we identify a set of three serine/threonine protein kinases (glycogen synthase kinase 3α/β [GSK3α/β], casein kinase 2 [CK2], and cyclin-dependent kinases 1/2 [CDK1/2]) that are, collectively, both necessary and sufficient to phosphorylate the triple serine motif. We show that phosphorylation of the motif itself serves as a template to prime phosphorylation of additional serines and creates a highly charged “acid blob” in the amino terminus of Olig2. Finally, we show that small molecule inhibitors of this forward-feeding phosphorylation cascade have potential as glioma therapeutics. [ABSTRACT FROM AUTHOR]

Published
2017
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231. Vitamin D receptor regulates autophagy in the normal mammary gland and in luminal breast cancer cells.

Author

Tavera-Mendoza, Luz E., Westerling, Thomas, Libby, Eric, Marusyk, Andriy, Cato, Laura, Cassani, Raymundo, Cameron, Lisa A., Ficarro, Scott B., Marto, Jarrod A., Klawitter, Jelena, and Brown, Myles

Subjects
BREAST cancer, VITAMIN D receptors, EPIDEMIOLOGY, MAMMARY glands, AUTOPHAGY
Abstract

Women in North America have a one in eight lifetime risk of developing breast cancer (BC), and a significant proportion of these individuals will develop recurrent BC and will eventually succumb to the disease. Metastatic, therapy-resistant BC cells are refractory to cell death induced by multiple stresses. Here, we document that the vitamin D receptor (VDR) acts as a master transcriptional regulator of autophagy. Activation of the VDR by vitamin D induces autophagy and an autophagic transcriptional signature in BC cells that correlates with increased survival in patients; strikingly, this signature is present in the normal mammary gland and is progressively lost in patients with metastatic BC. A number of epidemiological studies have shown that sufficient vitamin D serum levels might be protective against BC. We observed that dietary vitamin D supplementation in mice increases basal levels of autophagy in the normal mammary gland, highlighting the potential of vitamin D as a cancer-preventive agent. These findings point to a role of vitamin D and the VDR in modulating autophagy and cell death in both the normal mammary gland and BC cells. [ABSTRACT FROM AUTHOR]

Published
2017
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232. Proteomic approaches to study ubiquitinomics.

Author

Sahu, Indrajit, Zhu, He, Buhrlage, Sara J., and Marto, Jarrod A.

Abstract

As originally described some 40 years ago, protein ubiquitination was thought to serve primarily as a static mark for protein degradation. In the ensuing years, it has become clear that 'ubiquitination' is a structurally diverse and dynamic post-translational modification and is intricately involved in a myriad of signaling pathways in all eukaryote cells. And like other key pathways in the functional proteome, ubiquitin signaling is often disrupted, sometimes severely so, in human pathophysiology. As a result of its central role in normal physiology and human disease, the ubiquitination field is now represented across the full landscape of biomedical research from fundamental structural and biochemical studies to translational and clinical research. In recent years, mass spectrometry has emerged as a powerful technology for the detection and characterization of protein ubiquitination. Herein we detail qualitative and quantitative proteomic methods using a compare/contrast approach to highlight their strengths and weaknesses. • The expanded ubiquitin landscape in eukaryotic cells • Biochemical enrichment methods for ubiquitinated conjugates or peptides • MS-based bottom-up approaches for ubiquitination site identification • Approaches to quantifying the stoichiometry of ubiquitination • Techniques to determine ubiquitin chain architecture [ABSTRACT FROM AUTHOR]

Published
2023
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234. SOX2 and p63 colocalize at genetic loci in squamous cell carcinomas.

Author

Watanabe, Hideo, Watanabe, Hideo, Ma, Qiuping, Peng, Shouyong, Adelmant, Guillaume, Swain, Danielle, Song, Wenyu, Fox, Cameron, Francis, Joshua M, Pedamallu, Chandra Sekhar, DeLuca, David S, Brooks, Angela N, Wang, Su, Que, Jianwen, Rustgi, Anil K, Wong, Kwok-kin, Ligon, Keith L, Liu, X Shirley, Marto, Jarrod A, Meyerson, Matthew, Bass, Adam J, Watanabe, Hideo, Watanabe, Hideo, Ma, Qiuping, Peng, Shouyong, Adelmant, Guillaume, Swain, Danielle, Song, Wenyu, Fox, Cameron, Francis, Joshua M, Pedamallu, Chandra Sekhar, DeLuca, David S, Brooks, Angela N, Wang, Su, Que, Jianwen, Rustgi, Anil K, Wong, Kwok-kin, Ligon, Keith L, Liu, X Shirley, Marto, Jarrod A, Meyerson, Matthew, and Bass, Adam J

Abstract

The transcription factor SOX2 is an essential regulator of pluripotent stem cells and promotes development and maintenance of squamous epithelia. We previously reported that SOX2 is an oncogene and subject to highly recurrent genomic amplification in squamous cell carcinomas (SCCs). Here, we have further characterized the function of SOX2 in SCC. Using ChIP-seq analysis, we compared SOX2-regulated gene profiles in multiple SCC cell lines to ES cell profiles and determined that SOX2 binds to distinct genomic loci in SCCs. In SCCs, SOX2 preferentially interacts with the transcription factor p63, as opposed to the transcription factor OCT4, which is the preferred SOX2 binding partner in ES cells. SOX2 and p63 exhibited overlapping genomic occupancy at a large number of loci in SCCs; however, coordinate binding of SOX2 and p63 was absent in ES cells. We further demonstrated that SOX2 and p63 jointly regulate gene expression, including the oncogene ETV4, which was essential for SOX2-amplified SCC cell survival. Together, these findings demonstrate that the action of SOX2 in SCC differs substantially from its role in pluripotency. The identification of the SCC-associated interaction between SOX2 and p63 will enable deeper characterization the downstream targets of this interaction in SCC and normal squamous epithelial physiology.

Published
2014

235. Mutations in G protein β subunits promote transformation and kinase inhibitor resistance

Author

Yoda, Akinori, primary, Adelmant, Guillaume, additional, Tamburini, Jerome, additional, Chapuy, Bjoern, additional, Shindoh, Nobuaki, additional, Yoda, Yuka, additional, Weigert, Oliver, additional, Kopp, Nadja, additional, Wu, Shuo-Chieh, additional, Kim, Sunhee S, additional, Liu, Huiyun, additional, Tivey, Trevor, additional, Christie, Amanda L, additional, Elpek, Kutlu G, additional, Card, Joseph, additional, Gritsman, Kira, additional, Gotlib, Jason, additional, Deininger, Michael W, additional, Makishima, Hideki, additional, Turley, Shannon J, additional, Javidi-Sharifi, Nathalie, additional, Maciejewski, Jaroslaw P, additional, Jaiswal, Siddhartha, additional, Ebert, Benjamin L, additional, Rodig, Scott J, additional, Tyner, Jeffrey W, additional, Marto, Jarrod A, additional, Weinstock, David M, additional, and Lane, Andrew A, additional

Published
2014
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237. GNB1 Activating Mutations Promote Myeloid and Lymphoid Neoplasms Targetable By Combined PI3K/mTOR Inhibition

Author

Yoda, Akinori, primary, Adelmant, Guillaume, additional, Tamburini, Jerome, additional, Chapuy, Bjoern, additional, Shindoh, Nobuaki, additional, Yoda, Yuka, additional, Weigert, Oliver, additional, Kopp, Nadja, additional, Wu, Shuo-Chieh, additional, Kim, Sunhee S., additional, Liu, Huiyun, additional, Tivey, Trevor, additional, Christie, Amanda L, additional, Elpek, Kutlu G, additional, Card, Joseph, additional, Gritsman, Kira, additional, Gotlib, Jason, additional, Deininger, Michael W., additional, Makishima, Hideki, additional, Turley, Shannon, additional, Javidi-Sharifi, Nathalie, additional, Maciejewski, Jaroslaw P., additional, Rodig, Scott J, additional, Tyner, Jeffrey W., additional, Marto, Jarrod A, additional, Weinstock, David M., additional, and Lane, Andrew A., additional

Published
2014
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239. PARP1-Driven Poly-ADP-Ribosylation Regulates BRCA1 Function in Homologous Recombination–Mediated DNA Repair

Author

Hu, Yiduo, primary, Petit, Sarah A., additional, Ficarro, Scott B., additional, Toomire, Kimberly J., additional, Xie, Anyong, additional, Lim, Elgene, additional, Cao, Shiliang A., additional, Park, Eunyoung, additional, Eck, Michael J., additional, Scully, Ralph, additional, Brown, Myles, additional, Marto, Jarrod A., additional, and Livingston, David M., additional

Published
2014
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240. Identification of Kinase Inhibitor Targets in the Lung Cancer Microenvironment by Chemical and Phosphoproteomics

Author

Gridling, Manuela, primary, Ficarro, Scott B., additional, Breitwieser, Florian P., additional, Song, Lanxi, additional, Parapatics, Katja, additional, Colinge, Jacques, additional, Haura, Eric B., additional, Marto, Jarrod A., additional, Superti-Furga, Giulio, additional, Bennett, Keiryn L., additional, and Rix, Uwe, additional

Published
2014
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241. Pharmacological targeting of the pseudokinase Her3

Author

Xie, Ting, primary, Lim, Sang Min, additional, Westover, Kenneth D, additional, Dodge, Michael E, additional, Ercan, Dalia, additional, Ficarro, Scott B, additional, Udayakumar, Durga, additional, Gurbani, Deepak, additional, Tae, Hyun Seop, additional, Riddle, Steven M, additional, Sim, Taebo, additional, Marto, Jarrod A, additional, Jänne, Pasi A, additional, Crews, Craig M, additional, and Gray, Nathanael S, additional

Published
2014
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242. Abstract 1391: SOX2-p63 interaction and genomic co-localization in squamous cell carcinomas

Author

Watanabe, Hideo, primary, Ma, Qiuping, additional, Peng, Shouyong, additional, Adelmant, Guillaume, additional, Swain, Danielle, additional, Song, Wenyu, additional, Fox, Cameron, additional, Francis, Joshua M., additional, Pedamallu, Chandra Sekhar, additional, Deluca, David S., additional, Brooks, Angela N., additional, Que, Jianwen, additional, Rustgi, Anil K., additional, Wong, Kwok-kin, additional, Ligon, Keith L., additional, Liu, X. Shirley, additional, Marto, Jarrod A., additional, Meyerson, Matthew, additional, and Bass, Adam J., additional

Published
2014
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244. Systematic screening reveals a role for BRCA1 in the response to transcription-associated DNA damage

Author

Hill, Sarah J., primary, Rolland, Thomas, additional, Adelmant, Guillaume, additional, Xia, Xianfang, additional, Owen, Matthew S., additional, Dricot, Amélie, additional, Zack, Travis I., additional, Sahni, Nidhi, additional, Jacob, Yves, additional, Hao, Tong, additional, McKinney, Kristine M., additional, Clark, Allison P., additional, Reyon, Deepak, additional, Tsai, Shengdar Q., additional, Joung, J. Keith, additional, Beroukhim, Rameen, additional, Marto, Jarrod A., additional, Vidal, Marc, additional, Gaudet, Suzanne, additional, Hill, David E., additional, and Livingston, David M., additional

Published
2014
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246. Targeting transcription regulation in cancer with a covalent CDK7 inhibitor

Author

Kwiatkowski, Nicholas, primary, Zhang, Tinghu, additional, Rahl, Peter B., additional, Abraham, Brian J., additional, Reddy, Jessica, additional, Ficarro, Scott B., additional, Dastur, Anahita, additional, Amzallag, Arnaud, additional, Ramaswamy, Sridhar, additional, Tesar, Bethany, additional, Jenkins, Catherine E., additional, Hannett, Nancy M., additional, McMillin, Douglas, additional, Sanda, Takaomi, additional, Sim, Taebo, additional, Kim, Nam Doo, additional, Look, Thomas, additional, Mitsiades, Constantine S., additional, Weng, Andrew P., additional, Brown, Jennifer R., additional, Benes, Cyril H., additional, Marto, Jarrod A., additional, Young, Richard A., additional, and Gray, Nathanael S., additional

Published
2014
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250. SOX2 and p63 colocalize at genetic loci in squamous cell carcinomas

Author

Watanabe, Hideo, primary, Ma, Qiuping, additional, Peng, Shouyong, additional, Adelmant, Guillaume, additional, Swain, Danielle, additional, Song, Wenyu, additional, Fox, Cameron, additional, Francis, Joshua M., additional, Pedamallu, Chandra Sekhar, additional, DeLuca, David S., additional, Brooks, Angela N., additional, Wang, Su, additional, Que, Jianwen, additional, Rustgi, Anil K., additional, Wong, Kwok-kin, additional, Ligon, Keith L., additional, Liu, X. Shirley, additional, Marto, Jarrod A., additional, Meyerson, Matthew, additional, and Bass, Adam J., additional

Published
2014
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