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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
Journal Article
Cancer Cell, ISSN 1535-6108, 2010, Volume 17, Issue 6, pp. 547 - 559
In mice, Lkb1 deletion and activation of Kras G12D results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these... 
CELLCYCLE | SIGNALING | INACTIVATION | SUPPRESSOR | SIGNATURES | ONCOLOGY | SRC | ADENOCARCINOMA | SENSITIVITY | MUTATIONS | LKB1/STK11 | EXPRESSION | TUMORIGENESIS | CELL BIOLOGY | 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
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 06/2012, Volume 287, Issue 25, pp. 21509 - 21519
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 05/2017, Volume 24, Issue 5, pp. 889 - 902
Hepatocellular carcinoma (HCC) is the most common type of liver cancer in humans. The focal adhesion tyrosine kinase (FAK) is often over-expressed in human HCC... 
OVEREXPRESSION | METHYLATION | PROTEIN | INHIBITION | PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | NUCLEAR FAK | MECHANISMS | HISTONE METHYLTRANSFERASE EZH2 | CANCER | EXPRESSION | CELL BIOLOGY | Focal Adhesion Kinase 1 - genetics | Neoplasm Transplantation | RNA, Small Interfering - genetics | E2F2 Transcription Factor - genetics | Apoptosis - drug effects | Humans | Gene Expression Regulation, Neoplastic | Apoptosis - genetics | Male | Receptor, Notch2 - genetics | E2F2 Transcription Factor - metabolism | Tumor Suppressor Protein p53 - genetics | Carcinoma, Hepatocellular - genetics | Liver Neoplasms - pathology | Focal Adhesion Kinase 1 - metabolism | Promoter Regions, Genetic | Enhancer of Zeste Homolog 2 Protein - genetics | Enhancer of Zeste Homolog 2 Protein - metabolism | Liver Neoplasms - genetics | Signal Transduction | Receptor, Notch2 - metabolism | Tumor Suppressor Protein p53 - metabolism | E2F3 Transcription Factor - genetics | G2 Phase Cell Cycle Checkpoints | Hep G2 Cells | Animals | Histones - genetics | Mice, Nude | Aminopyridines - pharmacology | Carcinoma, Hepatocellular - pathology | E2F3 Transcription Factor - metabolism | Liver Neoplasms - metabolism | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Histones - metabolism | Focal Adhesion Kinase 1 - antagonists & inhibitors | Carcinoma, Hepatocellular - metabolism | RNA, Small Interfering - metabolism | Original Paper
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 7/2012, Volume 109, Issue 31, pp. 12562 - 12567
Journal Article
PLoS ONE, ISSN 1932-6203, 06/2012, Volume 7, Issue 6, p. e40148
The insulin-like growth factor receptor I (IGF-IR) plays an essential role in transformation by promoting cell growth and protecting cancer cells from... 
TRANSFORMATION | ACTIVATION | PROEPITHELIN | ERK1/2 | ADHESION KINASE | MULTIDISCIPLINARY SCIENCES | BLADDER-CANCER CELLS | GROWTH-FACTOR | DIFFERENTIATION | INSULIN-RECEPTOR SUBSTRATE-1 | NUCLEAR TRANSLOCATION | Paxillin - metabolism | Focal Adhesion Kinase 1 - genetics | Receptor, IGF Type 1 - metabolism | Paxillin - genetics | Urothelium - metabolism | Humans | Urinary Bladder Neoplasms - enzymology | Insulin-Like Growth Factor I - genetics | Insulin Receptor Substrate Proteins - metabolism | Cell Movement - genetics | Proto-Oncogene Proteins c-akt - genetics | Urothelium - pathology | Focal Adhesion Kinase 2 - genetics | Urinary Bladder Neoplasms - genetics | Focal Adhesion Kinase 2 - metabolism | Carcinoma - enzymology | GRB2 Adaptor Protein - genetics | Urinary Bladder Neoplasms - pathology | Urothelium - enzymology | Carcinoma - pathology | Insulin Receptor Substrate Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | Focal Adhesion Kinase 1 - metabolism | Urinary Bladder Neoplasms - metabolism | Neoplasm Invasiveness | Signal Transduction - genetics | Receptor, IGF Type 1 - genetics | Focal Adhesions - genetics | Focal Adhesions - metabolism | Cell Line, Tumor | Carcinoma - genetics | Mitogen-Activated Protein Kinases - genetics | Carcinoma - metabolism | GRB2 Adaptor Protein - metabolism | Insulin-Like Growth Factor I - metabolism | Mitogen-Activated Protein Kinases - metabolism | Tyrosine | Proline | Phenols | Carcinoma | Cancer | Transformation | Motility | Insulin-like growth factor I | Bladder | Homology | AKT protein | Biology | Insulin-like growth factors | Kinases | Tissues | Nuclei | Urology | Cell growth | Urinary bladder | Rodents | Cell cycle | Fibroblasts | Urothelial carcinoma | Localization | Protein-tyrosine kinase | Antigens | Urothelial cancer | Invasiveness | Proline-rich tyrosine kinase 2 | MAP kinase | Breast cancer | Insulin | Bladder cancer | Pathology | Signaling | Medical prognosis | Biomarkers | Diagnostic systems | Focal adhesion kinase | Immunofluorescence | Paxillin | Prostate cancer | Endocrinology | Apoptosis | Tumors
Journal Article
The Journal of Pathology, ISSN 0022-3417, 07/2017, Volume 242, Issue 3, pp. 358 - 370
Focal adhesion kinase (FAK) inhibitors have been developed as potential anticancer agents and are undergoing clinical trials. In vitro activation of the FAK... 
tumour angiogenesis | focal adhesion kinase | LOCALIZATION | ACTIVATION | PERMEABILITY | PHOSPHORYLATION | BARRIER FUNCTION | TUMOR ANGIOGENESIS | PATHOLOGY | SRC-FAMILY KINASES | CANCER | ONCOLOGY | SMOOTH-MUSCLE-CELLS | AUTOPHOSPHORYLATION | Cell Division - genetics | Focal Adhesion Kinase 1 - genetics | Neoplasm Transplantation | Antineoplastic Agents, Hormonal - pharmacology | Melanoma - blood supply | Focal Adhesion Protein-Tyrosine Kinases - metabolism | Capillary Permeability - drug effects | Melanoma - enzymology | Endothelium, Vascular - enzymology | Focal Adhesion Protein-Tyrosine Kinases - deficiency | Mutation - genetics | Capillary Permeability - genetics | Focal Adhesion Protein-Tyrosine Kinases - genetics | Homozygote | Neovascularization, Pathologic - enzymology | Animals | Melanoma - genetics | Tamoxifen - pharmacology | Cell Line, Tumor | Neovascularization, Pathologic - genetics | Mice | Cell Hypoxia - genetics | Focal Adhesion Kinase 1 - metabolism | Tyrosine | Fibronectins | Platelet-derived growth factor | Endothelial growth factors | Analysis | Melanoma | Phenols | Genetic aspects | Neovascularization | Permeability | Endothelium | Residues | Phosphorylation | Clinical trials | Activation | Kinases | Blood | Fibronectin | Anticancer properties | Angiogenesis | Antitumor agents | Leakage | Medical research | Vessels | Blood vessels | Tamoxifen | Cadherin | Src protein | Adhesion | Pathology | Signaling | Inhibitors | Hypoxia | In vivo methods and tests | Mutation | Focal adhesion kinase | Paxillin | In vitro methods and tests | Tumors | Original Paper | Original Papers
Journal Article
Nature Cell Biology, ISSN 1465-7392, 02/2004, Volume 6, Issue 2, pp. 154 - 161
Journal Article
American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 10/2013, Volume 49, Issue 4, pp. 536 - 543
Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase involved in various biological functions, including cell survival, proliferation, migration, and... 
Fibroblast | Pulmonary fibrosis | Focal adhesion kinase | T-CELL MIGRATION | LUNG FIBROSIS | TGF-BETA | COLLAGEN | CANCER CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MYOFIBROBLAST | CELL BIOLOGY | FAK | IN-VITRO | fibroblast | focal adhesion kinase | RESPIRATORY SYSTEM | pulmonary fibrosis | IMATINIB | GROWTH-FACTOR | Focal Adhesion Kinase 1 - genetics | Epithelial Cells - metabolism | Epithelial Cells - drug effects | Actins - metabolism | Insulin-Like Growth Factor I - genetics | Pulmonary Fibrosis - genetics | Platelet-Derived Growth Factor - genetics | Actins - genetics | Myofibroblasts - metabolism | Cell Differentiation - genetics | Phosphorylation - genetics | Bleomycin | Collagen Type I - genetics | Female | Pulmonary Fibrosis - metabolism | Phosphorylation - drug effects | Focal Adhesion Kinase 1 - metabolism | Fibroblasts - metabolism | Collagen Type I - metabolism | Mice, Inbred C57BL | Mesenchymal Stromal Cells - metabolism | Morpholines - pharmacology | DNA - metabolism | Myofibroblasts - drug effects | Platelet-Derived Growth Factor - metabolism | Tyrosine - metabolism | Animals | Transforming Growth Factor beta - genetics | Cell Differentiation - drug effects | Fibroblasts - drug effects | Pulmonary Fibrosis - chemically induced | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Pulmonary Fibrosis - drug therapy | Focal Adhesion Kinase 1 - antagonists & inhibitors | Transforming Growth Factor beta - metabolism | Insulin-Like Growth Factor I - metabolism | Tyrosine - genetics
Journal Article