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1. Full Text The Global Phosphorylation Landscape of SARS-CoV-2 Infection
by Bouhaddou, Mehdi and Memon, Danish and Meyer, Bjoern and White, Kris M and Rezelj, Veronica V and Correa Marrero, Miguel and Polacco, Benjamin J and Melnyk, James E and Ulferts, Svenja and Kaake, Robyn M and Batra, Jyoti and Richards, Alicia L and Stevenson, Erica and Gordon, David E and Rojc, Ajda and Obernier, Kirsten and Fabius, Jacqueline M and Soucheray, Margaret and Miorin, Lisa and Moreno, Elena and Koh, Cassandra and Tran, Quang Dinh and Hardy, Alexandra and Robinot, Rémy and Vallet, Thomas and Nilsson-Payant, Benjamin E and Hernandez-Armenta, Claudia and Dunham, Alistair and Weigang, Sebastian and Knerr, Julian and Modak, Maya and Quintero, Diego and Zhou, Yuan and Dugourd, Aurelien and Valdeolivas, Alberto and Patil, Trupti and Li, Qiongyu and Hüttenhain, Ruth and Cakir, Merve and Muralidharan, Monita and Kim, Minkyu and Jang, Gwendolyn and Tutuncuoglu, Beril and Hiatt, Joseph and Guo, Jeffrey Z and Xu, Jiewei and Bouhaddou, Sophia and Mathy, Christopher J.P and Gaulton, Anna and Manners, Emma J and Félix, Eloy and Shi, Ying and Goff, Marisa and Lim, Jean K and McBride, Timothy and O’Neal, Michael C and Cai, Yiming and Chang, Jason C.J and Broadhurst, David J and Klippsten, Saker and De wit, Emmie and Leach, Andrew R and Kortemme, Tanja and Shoichet, Brian and Ott, Melanie and Saez-Rodriguez, Julio and tenOever, Benjamin R and Mullins, R. Dyche and Fischer, Elizabeth R and Kochs, Georg and Grosse, Robert and García-Sastre, Adolfo and Vignuzzi, Marco and Johnson, Jeffery R and Shokat, Kevan M and Swaney, Danielle L and Beltrao, Pedro and Krogan, Nevan J
Cell (Cambridge), ISSN 0092-8674, 08/2020, Volume 182, Issue 3, pp. 685 - 712.e19
phosphoproteomics | SARS-CoV-2 | PIKFYVE | p38 | AXL | antiviral | casein kinase II | mass spectrometry | CDK | MAPK | Biochemistry & Molecular Biology | Life Sciences & Biomedicine | Science & Technology | Cell Biology | Phosphorylation | Cyclin-Dependent Kinases - metabolism | Pandemics | Humans | Phosphatidylinositol 3-Kinases - metabolism | COVID-19 | Pneumonia, Viral - metabolism | Peptidyl-Dipeptidase A - genetics | Coronavirus Infections - metabolism | HEK293 Cells | Peptidyl-Dipeptidase A - metabolism | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | p38 Mitogen-Activated Protein Kinases - metabolism | Cyclin-Dependent Kinases - antagonists & inhibitors | Proteomics - methods | Vero Cells | Caco-2 Cells | Phosphoinositide-3 Kinase Inhibitors - pharmacology | Proto-Oncogene Proteins - metabolism | A549 Cells | Drug Evaluation, Preclinical - methods | Proto-Oncogene Proteins - antagonists & inhibitors | Antiviral Agents - pharmacology | Chlorocebus aethiops | Spike Glycoprotein, Coronavirus - metabolism | Casein Kinase II - antagonists & inhibitors | Betacoronavirus - metabolism | Receptor Protein-Tyrosine Kinases - metabolism | Host-Pathogen Interactions | Angiotensin-Converting Enzyme 2 | Animals | Coronavirus Infections - virology | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | Pneumonia, Viral - virology | Casein Kinase II - metabolism | Antiviral agents | Viral proteins | Casein | Severe acute respiratory syndrome | Analysis | Coronaviruses | Health aspects | Mass spectrometry | Index Medicus
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2. Full Text The phosphoinositide 3′-kinase delta inhibitor, CAL-101, inhibits B-cell receptor signaling and chemokine networks in chronic lymphocytic leukemia
by Hoellenriegel, Julia and Meadows, Sarah A and Sivina, Mariela and Wierda, William G and Kantarjian, Hagop and Keating, Michael J and Giese, Neill and O'Brien, Susan and Yu, Albert and Miller, Langdon L and Lannutti, Brian J and Burger, Jan A
Blood, ISSN 0006-4971, 09/2011, Volume 118, Issue 13, pp. 3603 - 3612
Life Sciences & Biomedicine | Hematology | Science & Technology | Hematologic and hematopoietic diseases | Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis | Biological and medical sciences | Medical sciences | Cell Survival - drug effects | Phosphoinositide-3 Kinase Inhibitors | Purines - pharmacology | Humans | Cells, Cultured | Antineoplastic Agents - therapeutic use | Receptors, Antigen, B-Cell - antagonists & inhibitors | Down-Regulation - drug effects | Leukemia, Lymphocytic, Chronic, B-Cell - pathology | Cell Movement - drug effects | Class I Phosphatidylinositol 3-Kinases | Chemokines - antagonists & inhibitors | Signal Transduction - drug effects | Leukemia, Lymphocytic, Chronic, B-Cell - metabolism | Metabolic Networks and Pathways - physiology | Chemokines - metabolism | Purines - therapeutic use | Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy | Metabolic Networks and Pathways - drug effects | Quinazolinones - therapeutic use | Drug Evaluation, Preclinical | Quinazolinones - pharmacology | Index Medicus | Abridged Index Medicus | Lymphoid Neoplasia
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3. Full Text An epithelial-mesenchymal transition gene signature predicts resistance to EGFR and PI3K inhibitors and identifies Axl as a therapeutic target for overcoming EGFR inhibitor resistance
by Byers, Lauren Averett and Diao, Lixia and Wang, Jing and Saintigny, Pierre and Girard, Luc and Peyton, Michael and Shen, Li and Fan, Youhong and Giri, Uma and Tumula, Praveen K and Nilsson, Monique B and Gudikote, Jayanthi and Tran, Hai and Cardnell, Robert J. G and Bearss, David J and Warner, Steven L and Foulks, Jason M and Kanner, Steven B and Gandhi, Varsha and Krett, Nancy and Rosen, Steven T and Kim, Edward S and Herbst, Roy S and Blumenschein, George R and Lee, J. Jack and Lippman, Scott M and Ang, K. Kian and Mills, Gordon B and Hong, Waun K and Weinstein, John N and Wistuba, Ignacio I and Coombes, Kevin R and Minna, John D and Heymach, John V
Clinical cancer research, ISSN 1078-0432, 01/2013, Volume 19, Issue 1, pp. 279 - 290
Life Sciences & Biomedicine | Oncology | Science & Technology | Biological and medical sciences | Medical sciences | Antineoplastic agents | Pharmacology. Drug treatments | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Lung Neoplasms - drug therapy | Proto-Oncogene Proteins - antagonists & inhibitors | Recurrence | Phosphoinositide-3 Kinase Inhibitors | Reproducibility of Results | ErbB Receptors - antagonists & inhibitors | Carcinoma, Non-Small-Cell Lung - genetics | Humans | Lung Neoplasms - pathology | Proteome | Gene Expression Profiling | Epithelial-Mesenchymal Transition - genetics | Drug Resistance, Neoplasm - genetics | Neoplasm Metastasis | Animals | Proteomics | Cell Line, Tumor | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Mice | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Cluster Analysis | Index Medicus | lung cancer | EGFR inhibition | PI3K inhibition | Axl | EMT
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4. Full Text Sensitivity to PI3K and AKT inhibitors is mediated by divergent molecular mechanisms in subtypes of DLBCL
by Erdmann, Tabea and Klener, Pavel and Lynch, James T and Grau, Michael and Vočková, Petra and Molinsky, Jan and Tuskova, Diana and Hudson, Kevin and Polanska, Urszula M and Grondine, Michael and Mayo, Michele and Dai, Beiying and Pfeifer, Matthias and Erdmann, Kristian and Schwammbach, Daniela and Zapukhlyak, Myroslav and Staiger, Annette M and Ott, German and Berdel, Wolfgang E and Davies, Barry R and Cruzalegui, Francisco and Trneny, Marek and Lenz, Peter and Barry, Simon T and Lenz, Georg
Blood, ISSN 0006-4971, 07/2017, Volume 130, Issue 3, pp. 310 - 322
Life Sciences & Biomedicine | Hematology | Science & Technology | Phosphoinositide-3 Kinase Inhibitors | Apoptosis - drug effects | Protein-Tyrosine Kinases - metabolism | Humans | Gene Expression Regulation, Neoplastic | NF-kappa B - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Proto-Oncogene Proteins c-akt - genetics | Protein-Tyrosine Kinases - genetics | Piperidines - pharmacology | Oxadiazoles - pharmacology | Antineoplastic Agents - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Pyrazoles - pharmacology | PTEN Phosphohydrolase - genetics | NF-kappa B - antagonists & inhibitors | PTEN Phosphohydrolase - deficiency | Lymphoma, Large B-Cell, Diffuse - drug therapy | Lymphoma, Large B-Cell, Diffuse - pathology | Signal Transduction | Pyrimidines - pharmacology | Organ Specificity | Proto-Oncogene Proteins c-myc - metabolism | Drug Synergism | Phosphatidylinositol 3-Kinases - genetics | Xenograft Model Antitumor Assays | Pyrroles - pharmacology | Animals | NF-kappa B - genetics | Agammaglobulinaemia Tyrosine Kinase | Lymphoma, Large B-Cell, Diffuse - classification | Proto-Oncogene Proteins c-myc - antagonists & inhibitors | Mice | Protein Kinase Inhibitors - pharmacology | Proto-Oncogene Proteins c-myc - genetics | Lymphoma, Large B-Cell, Diffuse - genetics | Drug Combinations | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Drug Screening Assays, Antitumor | Protein-Tyrosine Kinases - antagonists & inhibitors | Index Medicus | Abridged Index Medicus
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5. Full Text Combined inhibition of MEK and PI3K pathways overcomes acquired resistance to EGFR‐TKIs in non‐small cell lung cancer
by Sato, Hiroki and Yamamoto, Hiromasa and Sakaguchi, Masakiyo and Shien, Kazuhiko and Tomida, Shuta and Shien, Tadahiko and Ikeda, Hirokuni and Hatono, Minami and Torigoe, Hidejiro and Namba, Kei and Yoshioka, Takahiro and Kurihara, Eisuke and Ogoshi, Yusuke and Takahashi, Yuta and Soh, Junichi and Toyooka, Shinichi
Cancer science, ISSN 1347-9032, 10/2018, Volume 109, Issue 10, pp. 3183 - 3196
MEK inhibitor | compensatory activation | acquired resistance | non‐small cell lung cancer | PI3K inhibitor | non-small cell lung cancer | Life Sciences & Biomedicine | Oncology | Science & Technology | Lung Neoplasms - drug therapy | Phosphoinositide-3 Kinase Inhibitors | Humans | ErbB Receptors - genetics | Epithelial-Mesenchymal Transition - drug effects | Lung Neoplasms - pathology | Phosphatidylinositol 3-Kinases - metabolism | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Mitogen-Activated Protein Kinase Kinases - metabolism | Female | Pyrimidinones - pharmacology | Imidazoles - therapeutic use | Carcinoma, Non-Small-Cell Lung - pathology | Oxazepines - therapeutic use | ErbB Receptors - antagonists & inhibitors | Pyrimidinones - therapeutic use | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Imidazoles - pharmacology | Oxazepines - pharmacology | Drug Synergism | Xenograft Model Antitumor Assays | Drug Resistance, Neoplasm - genetics | Animals | Signal Transduction - drug effects | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Mice, Nude | Protein Kinase Inhibitors - therapeutic use | Cell Line, Tumor | Cell Proliferation - drug effects | Mice, Inbred BALB C | Protein Kinase Inhibitors - pharmacology | Pyridones - therapeutic use | Carcinoma, Non-Small-Cell Lung - drug therapy | Mutation | Pyridones - pharmacology | Drug Resistance, Neoplasm - drug effects | Lung cancer, Small cell | Cellular signal transduction | Epidermal growth factor | Analysis | Tyrosine | Phosphorylation | Epidermal growth factor receptors | Mesenchyme | Lung cancer | Extracellular signal-regulated kinase | Clinical trials | Non-small cell lung carcinoma | MAP kinase | AKT protein | Drug resistance | 1-Phosphatidylinositol 3-kinase | c-Met protein | Signal transduction | Cell activation | Cell growth | Feedback | Stem cells | Protein-tyrosine kinase | Apoptosis | Tumors | Index Medicus | Original
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