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Nature, ISSN 0028-0836, 05/2016, Volume 534, Issue 7605, pp. 55 - 62
Somatic mutations have been extensively characterized in breast cancer, but the effects of these genetic alterations on the proteomic landscape remain poorly... 
PATHWAYS | HETEROGENEITY | PIK3CA MUTATIONS | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | GENES | BIOLOGY | RECEPTOR | EXPRESSION | SIGNATURE | REVEALS | Protein Kinases - metabolism | Focal Adhesion Kinase 1 - genetics | Receptor, Epidermal Growth Factor - genetics | Protein Kinases - genetics | Cyclin-Dependent Kinases - metabolism | Receptor, ErbB-2 - genetics | Receptors, G-Protein-Coupled - metabolism | Genomics | Humans | Gene Expression Regulation, Neoplastic | Receptor, ErbB-2 - metabolism | Phosphoproteins - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - genetics | Tumor Suppressor Protein p53 - genetics | Breast Neoplasms - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - metabolism | Breast Neoplasms - enzymology | Receptor, Epidermal Growth Factor - metabolism | Phosphoproteins - analysis | Mass Spectrometry | src-Family Kinases - metabolism | Female | Cyclin-Dependent Kinases - genetics | Focal Adhesion Kinase 1 - metabolism | Chromosomes, Human, Pair 5 - genetics | Breast Neoplasms - classification | Chromosome Deletion | p21-Activated Kinases - genetics | Signal Transduction | Molecular Sequence Annotation | Calcium-Binding Proteins - deficiency | Phosphoproteins - genetics | Mutation - genetics | S-Phase Kinase-Associated Proteins - metabolism | p21-Activated Kinases - metabolism | Phosphatidylinositol 3-Kinases - genetics | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Proteomics | S-Phase Kinase-Associated Proteins - genetics | Receptors, G-Protein-Coupled - genetics | src-Family Kinases - genetics | Calcium-Binding Proteins - genetics | Breast cancer | Genetic aspects | Research | Oncology, Experimental | Cancer | Physiological aspects | Methods | Mutation (Biology) | Proteins | Gene amplification | Peptides | Protein expression | Genomes | Mutation | Kinases | Deoxyribonucleic acid--DNA | Tumors | Index Medicus
Journal Article
Cancer Cell, ISSN 1535-6108, 2010, Volume 17, Issue 6, pp. 547 - 559
In mice, deletion and activation of results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and... 
CELLCYCLE | SIGNALING | EPITHELIAL-MESENCHYMAL TRANSITION | ONCOGENIC K-RAS | CANCER-CELLS | SUPPRESSOR | GENE | ONCOLOGY | SRC | KINASE INHIBITOR | EXPRESSION PROFILES | MUTATIONS | TUMORIGENESIS | Lung Neoplasms - drug therapy | Protein-Serine-Threonine Kinases - deficiency | Protein-Tyrosine Kinases - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Genomics | Humans | Lung Neoplasms - metabolism | Gene Expression Profiling | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Cell Movement - genetics | Phosphorylation - genetics | RNA Interference | Gene Expression Regulation, Neoplastic - genetics | MAP Kinase Kinase 1 - antagonists & inhibitors | Carcinoma, Non-Small-Cell Lung - metabolism | Signal Transduction - genetics | Enzyme Inhibitors - therapeutic use | Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors | Focal Adhesion Protein-Tyrosine Kinases - genetics | Focal Adhesions - genetics | Signal Transduction - drug effects | Mice, Nude | Cell Line, Tumor | Mice | TOR Serine-Threonine Kinases | src-Family Kinases - genetics | Protein-Tyrosine Kinases - antagonists & inhibitors | ras Proteins - genetics | Lung Neoplasms - pathology | Cell Transdifferentiation - genetics | Protein-Tyrosine Kinases - genetics | Neoplasm Metastasis - drug therapy | Mice, Mutant Strains | Protein-Serine-Threonine Kinases - antagonists & inhibitors | src-Family Kinases - metabolism | Female | Drug Therapy, Combination | Lung Neoplasms - genetics | Cell Adhesion - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Focal Adhesion Protein-Tyrosine Kinases - metabolism | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | src-Family Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - genetics | Proto-Oncogene Proteins - genetics | Up-Regulation - genetics | Xenograft Model Antitumor Assays | Neoplasm Metastasis - genetics | Animals | MAP Kinase Kinase 2 - antagonists & inhibitors | Protein Kinase Inhibitors - therapeutic use | Focal Adhesions - metabolism | Proteomics | Protein Kinase Inhibitors - pharmacology | Oncology, Experimental | Analysis | Lung cancer | Development and progression | Metastasis | Research | Cancer | Index Medicus
Journal Article
Diabetes, ISSN 0012-1797, 02/2014, Volume 63, Issue 2, pp. 514 - 525
The number and activity of brown adipocytes are linked to the ability of mammals to resist body fat accumulation. In some conditions, certain white adipose... 
OBESITY | GENE | ENDOCRINOLOGY & METABOLISM | MUSCLE | RECEPTOR | PROLIFERATION | DIFFERENTIATION | EXPRESSION | FAT-CELL | EXERCISE | ADIPOSE-TISSUE | MAP Kinase Signaling System - physiology | Nitriles - pharmacology | Adipose Tissue, White - metabolism | Caenorhabditis elegans Proteins - metabolism | Adipocytes - cytology | Male | Adipocytes - drug effects | Extracellular Signal-Regulated MAP Kinases - metabolism | Recombinant Proteins | Extracellular Signal-Regulated MAP Kinases - genetics | Pichia - metabolism | Membrane Transport Proteins - genetics | Dietary Fats | Membrane Transport Proteins - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Butadienes - pharmacology | Fibronectins - pharmacology | Fibronectins - administration & dosage | Mice, Inbred C57BL | Rats | p38 Mitogen-Activated Protein Kinases - genetics | Imidazoles - pharmacology | 3T3-L1 Cells | Rats, Sprague-Dawley | Animals | Adipocytes - metabolism | Pichia - genetics | Protein Binding | Adipose Tissue, Brown - drug effects | Adipose Tissue, Brown - metabolism | Fibronectins - genetics | Mice | Pyridines - pharmacology | Mutation | Mitochondrial Uncoupling Proteins | Caenorhabditis elegans Proteins - genetics | Adipose Tissue, White - drug effects | Physiological research | Cellular signal transduction | Research | Identification and classification | Membrane proteins | Proteins | Homeostasis | Diabetes | Kinases | Genes | Cells | Index Medicus | Abridged Index Medicus
Journal Article
Nature, ISSN 0028-0836, 02/2012, Volume 482, Issue 7385, pp. 419 - 422
Journal Article
The Plant Cell, ISSN 1040-4651, 5/2012, Volume 24, Issue 5, pp. 2225 - 2236
Journal Article
Nature Immunology, ISSN 1529-2908, 03/2015, Volume 16, Issue 4, pp. 354 - 365
Interleukin 37 (IL-37) and IL-1R8 (SIGIRR or TIR8) are anti-inflammatory orphan members of the IL-1 ligand family and IL-1 receptor family, respectively. Here... 
CELLS | FAMILY-MEMBER | INFLAMMATION | TIR8/SIGIRR | INFECTION | IMMUNOLOGY | TOLL | INHIBITOR | EXPRESSION | NEGATIVE REGULATOR | MOLECULES | Inflammation - pathology | Interleukin-1 - genetics | RNA, Small Interfering - genetics | RNA-Binding Proteins - genetics | Humans | Receptors, Interleukin-1 - genetics | NF-kappa B - immunology | Receptor Protein-Tyrosine Kinases - immunology | Proto-Oncogene Proteins c-fyn - genetics | Signal Transduction - immunology | TOR Serine-Threonine Kinases - genetics | PTEN Phosphohydrolase - immunology | RNA, Small Interfering - immunology | Receptors, Interleukin-1 - deficiency | Leukocytes, Mononuclear - immunology | c-Mer Tyrosine Kinase | Interleukin-1 - immunology | Interleukin-18 Receptor alpha Subunit - genetics | Proto-Oncogene Proteins - immunology | Proto-Oncogene Proteins c-fyn - immunology | STAT3 Transcription Factor - genetics | Cell Line | PTEN Phosphohydrolase - genetics | Interleukin-18 Receptor alpha Subunit - immunology | Leukocytes, Mononuclear - drug effects | MAP Kinase Kinase Kinases - genetics | Receptors, Interleukin-1 - immunology | RNA-Binding Proteins - immunology | Gene Expression Regulation | Mice, Transgenic | Proto-Oncogene Proteins - genetics | Inflammation - immunology | Immunity, Innate | MAP Kinase Kinase Kinases - immunology | Interleukin-18 Receptor alpha Subunit - antagonists & inhibitors | Leukocytes, Mononuclear - pathology | TOR Serine-Threonine Kinases - immunology | Animals | NF-kappa B - genetics | Receptor Protein-Tyrosine Kinases - genetics | Lipopolysaccharides - pharmacology | Inflammation - genetics | Protein Binding | Mice | STAT3 Transcription Factor - immunology | Receptors, Interleukin-1 - antagonists & inhibitors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 03/2010, Volume 464, Issue 7287, pp. 431 - 435
Activating mutations in KRAS and BRAF are found in more than 30% of all human tumours and 40% of melanoma, respectively, thus targeting this pathway could have... 
SELECTIVE INHIBITOR | POTENT | EFFICACY | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | IN-VIVO | C-RAF | HETERODIMERIZATION | B-RAF | PROTEIN-KINASE KINASE | CANCER | Neoplasms - metabolism | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Diphenylamine - pharmacology | raf Kinases - antagonists & inhibitors | Humans | Protein Multimerization | ras Proteins - metabolism | Protein Transport - drug effects | Extracellular Signal-Regulated MAP Kinases - metabolism | raf Kinases - metabolism | Diphenylamine - analogs & derivatives | Mitogen-Activated Protein Kinase Kinases - metabolism | Adenosine Triphosphate - metabolism | Indoles - pharmacology | Benzamides - pharmacology | Cell Membrane - metabolism | raf Kinases - genetics | Cell Membrane - drug effects | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Pyrazoles - pharmacology | Protein Structure, Tertiary | Proto-Oncogene Proteins - metabolism | Cell Line | Indenes - pharmacology | raf Kinases - chemistry | Proto-Oncogene Proteins c-raf - genetics | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Neoplasms - enzymology | Proto-Oncogene Proteins - genetics | Enzyme Activation - drug effects | Sulfonamides - pharmacology | Proto-Oncogene Proteins c-raf - metabolism | Neoplasms - drug therapy | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | MAP Kinase Signaling System - drug effects | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Proto-Oncogene Proteins c-raf - deficiency | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Neoplasms - pathology | Ras genes | Growth | Physiological aspects | Cellular signal transduction | Genetic aspects | Research | Mitogen-activated protein kinases | Competition | Clinical trials | Enzymes | Kinases | Index Medicus | Proteins | Cellular | Inhibitors | Pathways | Tumours | Signalling | Dimerization
Journal Article
by Weinstein, John N and Akbani, Rehan and Broom, Bradley M and Wang, Wenyi and Verhaak, Roeland G. W and McConkey, David and Lerner, Seth and Morgan, Margaret and Creighton, Chad J and Smith, Carolyn and Cherniack, Andrew D and Kim, Jaegil and Pedamallu, Chandra Sekhar and Noble, Michael S and Al-Ahmadie, Hikmat A and Reuter, Victor E and Rosenberg, Jonathan E and F.Bajorin, Dean and Bochner, Bernard H and Solit, David B and Koppie, Theresa and Robinson, Brian and Gordenin, Dmitry A and Fargo, David and Klimczak, Leszek J and Roberts, Steven A and Au, Jessie and Laird, Peter W and Hinoue, Toshinori and Schultz, Nikolaus and Ramirez, Ricardo and Hansel, Donna and Hoadley, Katherine A and Kim, William Y and Damrauer, Jeffrey S and Baylin, Stephen B and Mungall, Andrew J and Robertson, A. Gordon and Chu, Andy and Kwiatkowski, David J and Sougnez, Carrie and Cibulskis, Kristian and Lichtenstein, Lee and Sivachenko, Andrey and Stewart, Chip and Lawrence, Michael S and Getz, Gad and Lander, Eric and Gabrie, Stacey B and Donehower, Lawrence and Carter, Scott L and Saksena, Gordon and Schumacher, Steven E and Freeman, Samuel S and Jung, Joonil and Bhatt, Ami S and Pugh, Trevor and Beroukhim, Rameen and Meyerson, Matthew and Ally, Adrian and Balasundaram, Miruna and Butterfield, Yaron S. N and Dhalla, Noreen and Hirst, Carrie and Holt, Robert A and Jones, Steven J. M and Lee, Darlene and Li, Haiyan I and Marra, Marco A and Mayo, Michael and Moore, Richard A and Schein, Jacqueline E and Sipahimalani, Payal and Tam, Angela and Thiessen, Nina and Wong, Tina and Wye, Natasja and Bowlby, Reanne and Chuah, Eric and Guin, Ranabir and Shen, Hui and Bootwalla, Moiz S and Triche Jr, Timothy and Lai, Phillip H and Van Den Berg, David J and Weisenberger, Daniel J and Balu, Saianand and Bodenheimer, Tom and Hoyle, Alan P and Jefferys, Stuart R and Meng, Shaowu and Mose, Lisle E and Simons, Janae V and Soloway, Mathew G and Wu, Junyuan and Parker, Joel S and Hayes, D. Neil and Roach, Jeffrey and Buda, Elizabeth and Jones, Corbin D and ... and Canc Genome Atlas Res Network and Cancer Genome Atlas Research Network and The Cancer Genome Atlas Research Network
Nature, ISSN 0028-0836, 2014, Volume 507, Issue 7492, pp. 315 - 322
Journal Article