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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
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 01/2019, Volume 116, Issue 3, pp. 1027 - 1032
Merkel cell polyomavirus (MCV) contributes to approximately 80% of all Merkel cell carcinomas (MCCs), a highly aggressive neuroendocrine carcinoma of the skin.... 
MDM2–MDM4 | Lenalidomide | Merkel cell carcinoma | Casein kinase 1 alpha | P53 | UBIQUITINATION | casein kinase 1 alpha | POLYOMAVIRUS | MULTIDISCIPLINARY SCIENCES | GROWTH | DEGRADATION | MDM2-MDM4 | lenalidomide | p53 | T-ANTIGEN | Tumor Virus Infections - genetics | Proto-Oncogene Proteins c-mdm2 - genetics | Humans | Polyomavirus Infections - metabolism | Tumor Suppressor Protein p53 - genetics | DNA-Binding Proteins - metabolism | Retinoblastoma Binding Proteins - genetics | Nuclear Proteins - genetics | Retinoblastoma Binding Proteins - metabolism | DNA Helicases - genetics | Proto-Oncogene Proteins c-mdm2 - antagonists & inhibitors | Proto-Oncogene Proteins c-mdm2 - metabolism | Tumor Virus Infections - pathology | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Tumor Virus Infections - metabolism | Carcinoma, Merkel Cell - genetics | Tumor Suppressor Protein p53 - metabolism | Ubiquitin-Protein Ligases - metabolism | Merkel cell polyomavirus - metabolism | Nuclear Proteins - metabolism | Proto-Oncogene Proteins - genetics | DNA-Binding Proteins - genetics | Polyomavirus Infections - pathology | DNA Helicases - metabolism | Nuclear Proteins - antagonists & inhibitors | Polyomavirus Infections - genetics | Carcinoma, Merkel Cell - metabolism | Merkel cell polyomavirus - genetics | Carcinoma, Merkel Cell - virology | Ubiquitin-Protein Ligases - genetics | Carcinoma, Merkel Cell - pathology | Physiological aspects | Care and treatment | Tumor proteins | Oncogenes | Chromatin | Carcinoma | p53 Protein | Antigen T (large) | Genes | Xenotransplantation | Viruses | Homology | Activation | Myc protein | Gene sequencing | Proteins | Rodents | Xenografts | MDM2 protein | Ribonucleic acid--RNA | Gene expression | Depletion | Inhibitors | Cell lines | Skin | Mutation | Cancer | Tumors | Apoptosis | Index Medicus | Biological Sciences
Journal Article
Oncogene, ISSN 0950-9232, 05/2013, Volume 32, Issue 19, pp. 2452 - 2462
Journal Article
Molecular Cell, ISSN 1097-2765, 10/2016, Volume 64, Issue 1, pp. 51 - 64
The tumor suppressor protein 53BP1, a pivotal regulator of DNA double-strand break (DSB) repair, was first identified as a p53-interacting protein over two... 
BRCT DOMAINS | ACTIVATION | STRAND BREAK REPAIR | RESECTION | DAMAGE-RESPONSE | BIOCHEMISTRY & MOLECULAR BIOLOGY | V(D)J RECOMBINATION | TUMOR-SUPPRESSOR | CLASS-SWITCH RECOMBINATION | P53 PATHWAY | PROTEINS | CELL BIOLOGY | Gamma Rays | Endonucleases - genetics | Tumor Suppressor p53-Binding Protein 1 - chemistry | RNA, Guide - genetics | RNA, Guide - metabolism | Humans | Protein Multimerization | CRISPR-Associated Protein 9 | Endonucleases - metabolism | DNA Breaks, Double-Stranded | Tumor Suppressor Protein p53 - genetics | MCF-7 Cells | Base Sequence | Clustered Regularly Interspaced Short Palindromic Repeats | Ubiquitin Thiolesterase - metabolism | Protein Interaction Domains and Motifs | Binding Sites | Tumor Suppressor p53-Binding Protein 1 - metabolism | Promoter Regions, Genetic | Protein Conformation, alpha-Helical | Tumor Suppressor p53-Binding Protein 1 - genetics | Signal Transduction | Bacterial Proteins - genetics | Gene Expression Regulation | Tumor Suppressor Protein p53 - metabolism | Ubiquitin Thiolesterase - genetics | Gene Editing | Protein Conformation, beta-Strand | DNA Repair | Protein Binding | Bacterial Proteins - metabolism | Tumor Suppressor Protein p53 - chemistry | Ubiquitin Thiolesterase - chemistry | Oligomers | Ubiquitin | Ionizing radiation | Chromatin | Proteases | Genes | Genomics | DNA | Tumor proteins | DNA repair | Index Medicus
Journal Article
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