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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
Journal Article
Blood, ISSN 0006-4971, 06/2010, Volume 115, Issue 23, pp. 4951 - 4962
Cocaine abuse hastens the neurodegeneration often associated with advanced HIV-1 infection. The mechanisms, in part, revolve around the neuroinflammatory... 
PROTEIN-KINASE-C | SIGNALING PATHWAYS | ENDOTHELIAL-CELLS | COCAINE | CHEMOATTRACTANT PROTEIN-1 | HUMAN-IMMUNODEFICIENCY-VIRUS | CHEMOKINE RECEPTORS | HEMATOLOGY | BLOOD-BRAIN-BARRIER | NF-KAPPA-B | HIV-1 INVASION | HIV-1 | Microglia - metabolism | Mitogen-Activated Protein Kinase Kinases - genetics | Dopamine Uptake Inhibitors - adverse effects | Membrane Microdomains - metabolism | Male | Monocytes - metabolism | NF-kappa B - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Cocaine-Related Disorders - genetics | Cell Movement - genetics | Brain - metabolism | Mitogen-Activated Protein Kinase Kinases - metabolism | Cocaine-Related Disorders - metabolism | MAP Kinase Signaling System - genetics | HIV Infections - pathology | Monocytes - pathology | src-Family Kinases - metabolism | Microglia - pathology | Chemokine CCL2 - metabolism | Cocaine - adverse effects | Receptors, sigma - metabolism | Neurodegenerative Diseases - pathology | Dopamine Uptake Inhibitors - pharmacology | Gene Expression Regulation - genetics | HIV Infections - genetics | Cocaine-Related Disorders - pathology | Rats | Chemokine CCL2 - genetics | Neurodegenerative Diseases - genetics | Receptors, sigma - genetics | Neurodegenerative Diseases - metabolism | Mice, Knockout | Gene Expression Regulation - drug effects | Phosphatidylinositol 3-Kinases - genetics | Cell Movement - drug effects | Cocaine - pharmacology | Animals | MAP Kinase Signaling System - drug effects | Neurodegenerative Diseases - chemically induced | NF-kappa B - genetics | Brain - pathology | Mice | src-Family Kinases - genetics | Membrane Microdomains - pathology | Membrane Microdomains - genetics | HIV Infections - metabolism | Index Medicus | Abridged Index Medicus | Vascular Biology | HIV Infections | Membrane Microdomains | Brain | pathology | src-Family Kinases | Cocaine-Related Disorders | Phosphatidylinositol 3-Kinases | MAP Kinase Signaling System | Receptors | genetics | Mitogen-Activated Protein Kinase Kinases | NF-kappa B | pharmacology | Dopamine Uptake Inhibitors | sigma | Neurodegenerative Diseases | chemically induced | Gene Expression Regulation | Cell and Molecular Biology | drug effects | Knockout | Microglia | Monocytes | adverse effects | metabolism | Cocaine | Chemokine CCL2 | Cell- och molekylärbiologi | Cell Movement
Journal Article
Blood, ISSN 0006-4971, 02/2017, Volume 129, Issue 6, pp. 759 - 770
Kinases downstream of B-cell antigen receptor (BCR) represent attractive targets for therapy in non-Hodgkin lymphoma (NHL). As clinical responses vary,... 
SURFACE IGM | BCR | CHRONIC-LYMPHOCYTIC-LEUKEMIA | BRUTONS TYROSINE KINASE | HUMAN FOLLICULAR LYMPHOMA | GENE-EXPRESSION | KINASE INHIBITOR IBRUTINIB | MUTATIONS | TARGETING BTK | HEMATOLOGY | NF-KAPPA-B | Lymphoma, Follicular - metabolism | Protein-Tyrosine Kinases - metabolism | Humans | Lymphoma, Mantle-Cell - pathology | Leukemia, Lymphocytic, Chronic, B-Cell - genetics | Receptors, Antigen, B-Cell - metabolism | STAT1 Transcription Factor - metabolism | Lymphoma, Follicular - genetics | Mitogen-Activated Protein Kinase 1 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Single-Cell Analysis | Immunoglobulin M - genetics | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | STAT1 Transcription Factor - genetics | Leukemia, Lymphocytic, Chronic, B-Cell - pathology | Lymphoma, Large B-Cell, Diffuse - diagnosis | Mitogen-Activated Protein Kinase 3 - metabolism | Leukemia, Lymphocytic, Chronic, B-Cell - metabolism | Receptors, Antigen, B-Cell - genetics | CD79 Antigens - genetics | src-Family Kinases - genetics | Mitogen-Activated Protein Kinase 1 - metabolism | Phosphorylation | Gene Expression Regulation, Neoplastic | Lymphoma, Follicular - diagnosis | Lymphoma, Large B-Cell, Diffuse - metabolism | Phosphoproteins - metabolism | Proto-Oncogene Proteins c-akt - genetics | Lymphoma, Mantle-Cell - diagnosis | STAT5 Transcription Factor - genetics | STAT5 Transcription Factor - metabolism | Protein-Tyrosine Kinases - genetics | Flow Cytometry | Syk Kinase - genetics | Phospholipase C gamma - genetics | src-Family Kinases - metabolism | Lymphoma, Mantle-Cell - genetics | Lymphoma, Mantle-Cell - metabolism | Diagnosis, Differential | Phospholipase C gamma - metabolism | Lymphoma, Large B-Cell, Diffuse - pathology | Lymphoma, Follicular - pathology | p38 Mitogen-Activated Protein Kinases - genetics | Phosphoproteins - genetics | CD79 Antigens - metabolism | Syk Kinase - metabolism | Lymphoma, Large B-Cell, Diffuse - genetics | Leukemia, Lymphocytic, Chronic, B-Cell - diagnosis | Index Medicus | Abridged Index Medicus | Life Sciences | Human health and pathology | Hematology | Cancer | Lymphoid Neoplasia
Journal Article
Nature Structural & Molecular Biology, ISSN 1545-9993, 10/2008, Volume 15, Issue 10, pp. 1109 - 1118
Journal Article
Biochemical Journal, ISSN 0264-6021, 02/2017, Volume 474, Issue 4, pp. 597 - 609
Cyclic AMP (cAMP)-specific phosphodiesterase-4 (PDE4) enzymes underpin compartmentalised cAMP signalling by localising to distinct signalling complexes. PDE4... 
CELLS | SIGNALING PATHWAYS | ACTIVATION | CAMP-SPECIFIC PHOSPHODIESTERASE | PROTEIN-KINASE | MAP KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | A-MEDIATED PHOSPHORYLATION | BETA-ARRESTIN | BINDING-SITES | ROLIPRAM INHIBITION | Humans | Cyclic AMP-Dependent Protein Kinases - chemistry | Intracellular Signaling Peptides and Proteins - metabolism | Cyclic AMP-Dependent Protein Kinases - genetics | Mitogen-Activated Protein Kinase 1 - genetics | Cyclic Nucleotide Phosphodiesterases, Type 4 - metabolism | Cyclic Nucleotide Phosphodiesterases, Type 4 - chemistry | Intracellular Signaling Peptides and Proteins - genetics | 1-Alkyl-2-acetylglycerophosphocholine Esterase - chemistry | Protein-Serine-Threonine Kinases - metabolism | Gene Expression | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Recombinant Proteins - chemistry | Ubiquitin-Conjugating Enzymes - genetics | Cyclic Nucleotide Phosphodiesterases, Type 4 - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Ubiquitin-Conjugating Enzymes - metabolism | Molecular Docking Simulation | Protein-Serine-Threonine Kinases - chemistry | src-Family Kinases - genetics | COS Cells | Mitogen-Activated Protein Kinase 1 - metabolism | Microtubule-Associated Proteins - chemistry | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | beta-Arrestins - metabolism | Cercopithecus aethiops | Ubiquitin-Conjugating Enzymes - chemistry | Mitogen-Activated Protein Kinase 1 - chemistry | 1-Alkyl-2-acetylglycerophosphocholine Esterase - genetics | HEK293 Cells | src-Family Kinases - metabolism | Protein Interaction Domains and Motifs | Mitogen-Activated Protein Kinase 3 - chemistry | beta-Arrestins - chemistry | Cyclic AMP-Dependent Protein Kinases - metabolism | Recombinant Proteins - metabolism | Catalytic Domain | Protein Structure, Secondary | Protein-Serine-Threonine Kinases - genetics | Recombinant Proteins - genetics | Amino Acid Motifs | 1-Alkyl-2-acetylglycerophosphocholine Esterase - metabolism | beta-Arrestins - genetics | Animals | Intracellular Signaling Peptides and Proteins - chemistry | Protein Binding | src-Family Kinases - chemistry | Index Medicus | protein–protein interactions | cAMP | cyclic nucleotide phosphodiesterases
Journal Article
Nature, ISSN 0028-0836, 01/2010, Volume 463, Issue 7277, pp. 88 - 92
Journal Article
Oncogene, ISSN 0950-9232, 05/2014, Volume 33, Issue 19, pp. 2495 - 2503
Journal Article
Nature Genetics, ISSN 1061-4036, 07/2016, Volume 48, Issue 7, pp. 747 - 757
Genome-wide association studies have identified several loci associated with pancreatic cancer risk; however, the mechanisms by which genetic factors influence... 
U-BOX | REGULATORY RNA | RETINOIC ACID | LONG NONCODING RNA | GENETICS & HEREDITY | SQUAMOUS-CELL CARCINOMA | GENE-EXPRESSION | SUSCEPTIBILITY LOCI | UBIQUITIN LIGASES | IDENTIFY MULTIPLE | GENOME-WIDE ASSOCIATION | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Cell Proliferation | Pancreatic Neoplasms - metabolism | Humans | DNA Repair Enzymes - genetics | Gene Expression Regulation, Neoplastic | Extracellular Signal-Regulated MAP Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - genetics | Case-Control Studies | RNA Splicing Factors - metabolism | STAT1 Transcription Factor - metabolism | Ubiquitination | Proteolysis | DNA Repair Enzymes - metabolism | src-Family Kinases - metabolism | Nuclear Proteins - genetics | Binding Sites | Genome-Wide Association Study | Signal Transduction | Pancreatic Neoplasms - pathology | Nuclear Proteins - metabolism | Pancreatic Neoplasms - genetics | RNA, Long Noncoding - genetics | Pancreas - metabolism | RNA Splicing Factors - genetics | STAT1 Transcription Factor - genetics | Polymorphism, Single Nucleotide - genetics | MicroRNAs - genetics | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics | src-Family Kinases - genetics | MicroRNA | Phosphatases | Genetic variation | Pancreatic cancer | Development and progression | Genetic aspects | Properties | Health aspects | Proteins | Studies | Confidence intervals | Research & development--R&D | Genomes | Mutation | Gene expression | Phosphatase | Cancer | Index Medicus
Journal Article