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Angewandte Chemie International Edition, ISSN 1433-7851, 08/2016, Volume 55, Issue 36, pp. 10612 - 10615
The design of inhibitors of intracellular protein–protein interactions (PPIs) remains a challenge in chemical biology and drug discovery. We propose a cyclized... 
protein–protein interactions | helix-loop-helix peptides | inhibitors | cell-penetrating peptides | epitope grafting | P53-MDM2 INTERACTION | DOMAIN | LIBRARY | CHEMISTRY, MULTIDISCIPLINARY | CANCER-THERAPY | protein-protein interactions | P53 | IN-VIVO ACTIVATION | MDM2 | ANTAGONISTS | SELECTION | TUMOR-SUPPRESSOR PATHWAY | Amino Acid Sequence | Protein Conformation, alpha-Helical | Tumor Suppressor Protein p53 - antagonists & inhibitors | Protein Interaction Maps - drug effects | Humans | Tumor Suppressor Protein p53 - metabolism | Peptides, Cyclic - pharmacology | Proto-Oncogene Proteins c-mdm2 - chemistry | Arginine - analogs & derivatives | Peptides, Cyclic - chemistry | Protein Interaction Mapping | Arginine - pharmacology | Drug Design | Cell Line, Tumor | Molecular Docking Simulation | Tumor Suppressor Protein p53 - chemistry | Proto-Oncogene Proteins c-mdm2 - antagonists & inhibitors | Proto-Oncogene Proteins c-mdm2 - metabolism | Peptides | Arginine | Drug discovery | Permeability | Tumor proteins | Protein-protein interactions | Antigenic determinants | Proteins | Binding | Residues | p53 Protein | Confocal microscopy | Biology | Confocal | Design analysis | Grafting | Design | Penetration | Inhibitors | Microscopy | Computer applications | Helix-loop-helix proteins | Inhibition | Intracellular | Position (location) | Localization | Protein interaction | Cancer | Index Medicus
Journal Article
Molecular and Cellular Biology, ISSN 0270-7306, 09/2018, Volume 38, Issue 17
RASSF6 is a member of the tumor suppressor Ras association domain family (RASSF) proteins. RASSF6 is frequently suppressed in human cancers, and its low... 
RB1 | Cell cycle arrest | Tumor suppressor | RASSF6 | Apoptosis | PROMOTER HYPERMETHYLATION | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | apoptosis | tumor suppressor | PROLIFERATION | HIPPO PATHWAY REGULATION | cell cycle arrest | CANCER | FAMILY | P53 | CELL BIOLOGY | E2F | EXPRESSION | Genomic Instability | Humans | Tumor Protein p73 - genetics | Apoptosis - genetics | Tumor Protein p73 - metabolism | Tumor Suppressor Protein p53 - genetics | Gene Knockdown Techniques | Genes, p53 | Tumor Suppressor Proteins - deficiency | Tumor Suppressor Proteins - genetics | HEK293 Cells | Cell Cycle Checkpoints - genetics | E2F1 Transcription Factor - antagonists & inhibitors | Retinoblastoma Binding Proteins - genetics | Retinoblastoma Binding Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Genes, Retinoblastoma | HCT116 Cells | Retinoblastoma Binding Proteins - deficiency | Tumor Suppressor Protein p53 - metabolism | Ubiquitin-Protein Ligases - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Cell Cycle Checkpoints - physiology | E2F1 Transcription Factor - metabolism | Monomeric GTP-Binding Proteins - genetics | Tumor Suppressor Protein p53 - deficiency | Monomeric GTP-Binding Proteins - deficiency | Monomeric GTP-Binding Proteins - metabolism | Models, Biological | DNA Repair | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Ubiquitin-Protein Ligases - deficiency | Apoptosis - physiology | HeLa Cells | Tumor Suppressor Protein p14ARF - genetics | E2F1 Transcription Factor - genetics | Tumor Suppressor Protein p14ARF - metabolism | Ubiquitin-Protein Ligases - genetics | Index Medicus
Journal Article
Journal Article
Cancer Cell, ISSN 1535-6108, 10/2007, Volume 12, Issue 4, pp. 342 - 354
The tumor suppressor p53 is a transcription factor that responds to cellular stresses by initiating cell cycle arrest or apoptosis. One transcriptional target... 
PROTEINS | CELLCYCLE | TRANSCRIPTIONAL ACTIVATION | CHK2 KINASE | PROTEIN | ONCOLOGY | DNA-DAMAGE RESPONSE | MDM2 | ATM | P53 PATHWAY | CELL-GROWTH | IONIZING-RADIATION | PPM1D | Protein-Serine-Threonine Kinases - deficiency | Fibroblasts - enzymology | Phosphorylation | Proto-Oncogene Proteins c-mdm2 - genetics | Humans | Phosphoprotein Phosphatases - metabolism | Ubiquitin - metabolism | Homeostasis | DNA-Binding Proteins - deficiency | Tumor Suppressor Protein p53 - genetics | DNA-Binding Proteins - metabolism | Transfection | RNA Interference | Time Factors | Tumor Suppressor Proteins - deficiency | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Ubiquitin Thiolesterase - metabolism | Transcription, Genetic | Signal Transduction - radiation effects | Proto-Oncogene Proteins c-mdm2 - metabolism | Osteosarcoma - metabolism | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Tumor Suppressor Proteins - metabolism | Osteosarcoma - enzymology | Cell Cycle Proteins - metabolism | Protein Phosphatase 2C | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Serine - metabolism | Mice, Knockout | Animals | Phosphoprotein Phosphatases - genetics | Fibroblasts - radiation effects | Cell Line, Tumor | Phosphoprotein Phosphatases - deficiency | Mice | DNA Damage | Mutation | Osteosarcoma - genetics | Proteasome Endopeptidase Complex - metabolism | Ubiquitin-Specific Peptidase 7 | RNA, Small Interfering - metabolism | Index Medicus
Journal Article
Nature Cell Biology, ISSN 1465-7392, 07/2004, Volume 6, Issue 7, pp. 665 - 672
The promyelocytic leukaemia (PML) tumour-suppressor protein potentiates p53 function by regulating post-translational modifications, such as CBP-dependent... 
APOPTOSIS | NUCLEAR-BODIES | PREMATURE SENESCENCE | INHIBITION | ONCOGENIC RAS | DNA-DAMAGE | SENSITIVITY | ATM | RIBOSOMAL-PROTEIN L11 | STRESS | CELL BIOLOGY | NIH 3T3 Cells | Phosphorylation | Humans | Neoplasm Proteins - metabolism | Tumor Suppressor Protein p53 - genetics | Ribosomal Proteins - metabolism | Cell Nucleolus - metabolism | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Fibroblasts | ADP-Ribosylation Factor 1 - metabolism | ADP-Ribosylation Factor 1 - genetics | Neoplasm Proteins - genetics | Nuclear Proteins - genetics | Active Transport, Cell Nucleus - genetics | Protein-Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Cell Nucleolus - genetics | Ribosomal Proteins - genetics | Cell Compartmentation - genetics | Cell Cycle Proteins - metabolism | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | Proto-Oncogene Proteins - genetics | Ataxia Telangiectasia Mutated Proteins | Transcription Factors - genetics | RNA Stability - genetics | Protein Transport - genetics | Transcription Factors - metabolism | Proto-Oncogene Proteins c-mdm2 | Animals | Mice | Cell Line, Transformed | Promyelocytic Leukemia Protein | Post-translational modification | Control | Myelocytic leukemia | Physiological aspects | Tumor suppressor genes | Genetic aspects | Nonlymphoid leukemia | Research | Risk factors | Index Medicus
Journal Article
Journal Article
Cell, ISSN 0092-8674, 2006, Volume 126, Issue 2, pp. 269 - 283
The PML tumor suppressor controls key pathways for growth suppression, induction of apoptosis, and cellular senescence. PML loss occurs frequently in human... 
APOPTOSIS | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | PROTEIN-KINASE CK2 | DNA-DAMAGE | GROWTH | SENESCENCE | NUCLEAR-BODY FORMATION | EXPRESSION | CARCINOMA | P53 | CELL BIOLOGY | NIH 3T3 Cells | Protein Subunits | Transcription Factors - chemistry | Humans | Transcriptional Activation | Ubiquitin - metabolism | Neoplasm Proteins - antagonists & inhibitors | Casein Kinase II - genetics | Tumor Suppressor Proteins - chemistry | p38 Mitogen-Activated Protein Kinases - metabolism | Neoplasm Proteins - genetics | Genes, Tumor Suppressor | Amino Acid Sequence | Tumor Suppressor Proteins - metabolism | Lung Neoplasms - enzymology | Enzyme Inhibitors - pharmacology | Mice, Transgenic | Neoplasm Proteins - chemistry | Nuclear Proteins - chemistry | Serine - metabolism | Leupeptins - pharmacology | Tumor Suppressor Proteins - physiology | Cell Line, Tumor | Mice | Carcinoma, Non-Small-Cell Lung - enzymology | Enzyme Activation | Proteasome Endopeptidase Complex - metabolism | Sequence Deletion | Phosphorylation | Tumor Suppressor Proteins - antagonists & inhibitors | Neoplasm Proteins - physiology | Molecular Sequence Data | Lung Neoplasms - pathology | Neoplasm Proteins - metabolism | Tumor Suppressor Proteins - genetics | Nuclear Proteins - genetics | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Protein Structure, Tertiary | Cell Line | Green Fluorescent Proteins - metabolism | Transcription Factors - physiology | Carcinoma, Non-Small-Cell Lung - genetics | RNA, Small Interfering - pharmacology | Casein Kinase II - antagonists & inhibitors | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Transcription Factors - genetics | Serine - chemistry | Transcription Factors - metabolism | Triazoles - pharmacology | Animals | Hemagglutinins - chemistry | Nuclear Proteins - antagonists & inhibitors | Nuclear Proteins - physiology | Casein Kinase II - metabolism | Cell Line, Transformed | Promyelocytic Leukemia Protein | Sorbitol - pharmacology | Amino Acid Substitution | Apoptosis | Genetic research | Tumor suppressor genes | Research | Protein kinases | Oncogenes | Prevention | Casein | Health aspects | Analysis | Lung cancer | Cancer | Index Medicus
Journal Article
PloS one, ISSN 1932-6203, 2013, Volume 8, Issue 10, pp. e77053 - e77053
Glioblastoma multiforme (GBM) is the most common primary brain cancer in adults and there are few effective treatments. GBMs contain cells with molecular and... 
CANCER-CELLS | SOLID TUMORS | MULTIDISCIPLINARY SCIENCES | INTEGRATED GENOMIC ANALYSIS | HUMAN GLIOMAS | IMAGE-BASED SCREENS | CENTRAL-NERVOUS-SYSTEM | BRAIN-BARRIER MODEL | ADHERENT CULTURE | PHASE-I | TUMOR-INITIATING CELLS | Small Molecule Libraries - pharmacology | Glioblastoma - enzymology | Neoplastic Stem Cells - drug effects | Humans | Brain Neoplasms - pathology | Brain Neoplasms - metabolism | Tumor Suppressor Protein p53 - genetics | Cell Cycle Proteins - antagonists & inhibitors | Glioblastoma - genetics | Swine | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Neoplastic Stem Cells - pathology | Protein-Serine-Threonine Kinases - metabolism | Pyrazoles - pharmacology | Proto-Oncogene Proteins - metabolism | Cell Survival - drug effects | Proto-Oncogene Proteins - antagonists & inhibitors | Pteridines - pharmacology | Drug Screening Assays, Antitumor - methods | Cell Cycle Proteins - metabolism | Cells, Cultured | Neural Stem Cells - drug effects | Protein-Serine-Threonine Kinases - genetics | Brain Neoplasms - genetics | Thiophenes - pharmacology | Proto-Oncogene Proteins - genetics | Reverse Transcriptase Polymerase Chain Reaction | Tumor Suppressor Protein p53 - deficiency | Blood-Brain Barrier - drug effects | Neural Stem Cells - enzymology | Neural Stem Cells - pathology | Blotting, Western | Blood-Brain Barrier - metabolism | Mice, Knockout | Animals | Cell Cycle Checkpoints - drug effects | Glioblastoma - pathology | Cell Line, Tumor | Benzimidazoles - pharmacology | Mice | Protein Kinase Inhibitors - pharmacology | Neoplastic Stem Cells - enzymology | Indans - pharmacology | Viral antibodies | Polo | Brain tumors | Stem cells | Antibodies | Tumor proteins | Glioblastoma multiforme | Neuroimaging | Image processing | Polo-like kinase 1 | Laboratories | p53 Protein | Brain cancer | Glioblastoma | Childrens health | Membrane permeability | Stem cell transplantation | Kinases | Cancer therapies | Defects | Allografts | Blood-brain barrier | Clonal deletion | DNA methylation | Deletion | Polo-like kinase | Cyclin-dependent kinase inhibitors | Pharmaceutical industry | Bioinformatics | Pharmaceutical sciences | Medical research | Antibody microarrays | INK4 protein | Permeability | Gene expression | Medical screening | Endothelial cells | Image analysis | Sensitivity | Brain research | Inhibitors | Neural stem cells | Adults | Mutation | Molecular biology | Human behavior | Tumors | Cancer | Index Medicus
Journal Article
Oncogene, ISSN 0950-9232, 05/2013, Volume 32, Issue 19, pp. 2452 - 2462
Journal Article