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Annual Review of Biochemistry, ISSN 0066-4154, 6/2016, Volume 85, Issue 1, pp. 375 - 404
Inactivation of the transcription factor p53, through either direct mutation or aberrations in one of its many regulatory pathways, is a hallmark of virtually... 
cancer therapy | signaling pathways | protein evolution | drug design | p53 family | small-molecule stabilizers | Protein evolution | Signaling pathways | Drug design | Small-molecule stabilizers | P53 family | Cancer therapy | DNA-BINDING DOMAIN | TRANSIENT PROTEIN STATES | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL-CYCLE ARREST | TUMOR-SUPPRESSOR P53 | CORE-DOMAIN | STRUCTURAL BASIS | SMALL-MOLECULE INHIBITORS | MUTANT P53 | TETRAMERIZATION DOMAIN | TRANSACTIVATION DOMAIN | Neoplasms - metabolism | Proto-Oncogene Proteins c-mdm2 - genetics | Antineoplastic Agents, Alkylating - chemical synthesis | Humans | Protein Multimerization | Gene Expression Regulation, Neoplastic | Proto-Oncogene Proteins - chemistry | Molecular Targeted Therapy | Proto-Oncogene Proteins c-mdm2 - chemistry | Tumor Suppressor Protein p53 - genetics | Neoplasms - genetics | Tumor Suppressor Protein p53 - agonists | Drug Design | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-mdm2 - antagonists & inhibitors | Proto-Oncogene Proteins c-mdm2 - metabolism | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Protein Structure, Secondary | Signal Transduction | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | Proto-Oncogene Proteins - genetics | Clinical Trials as Topic | Nuclear Proteins - chemistry | Neoplasms - drug therapy | Antineoplastic Agents, Alkylating - therapeutic use | Animals | Nuclear Proteins - antagonists & inhibitors | Molecular Docking Simulation | Tumor Suppressor Protein p53 - chemistry | Mutation | Neoplasms - pathology | Transcription factors | Care and treatment | Health aspects | Methods | Cancer
Journal Article
Nature Medicine, ISSN 1078-8956, 08/2012, Volume 18, Issue 8, pp. 1239 - 1247
The inactivation of the p53 tumor suppressor pathway, which often occurs through mutations in TP53 (encoding tumor protein 53) is a common step in human... 
MEDICINE, RESEARCH & EXPERIMENTAL | N-RAS | BIOCHEMISTRY & MOLECULAR BIOLOGY | TUMOR-SUPPRESSOR ACTIVITY | STAPLED P53 | BRAF | MALIGNANT-MELANOMA | P53 PATHWAY | CELL-DEATH | CELL BIOLOGY | BREAST-CANCER | METASTATIC MELANOMA | IN-VIVO | Up-Regulation | Proto-Oncogene Proteins c-mdm2 - genetics | Tumor Suppressor Protein p53 - antagonists & inhibitors | Apoptosis - drug effects | Humans | Neoplasm Proteins - physiology | Gene Expression Regulation, Neoplastic | Recombinant Fusion Proteins - physiology | Skin Neoplasms - chemistry | Male | Melanocytes - metabolism | Neoplasm Proteins - antagonists & inhibitors | Cell Line, Tumor - transplantation | Proto-Oncogene Proteins - biosynthesis | Tumor Suppressor Protein p53 - physiology | Cell-Penetrating Peptides - pharmacology | Nuclear Proteins - biosynthesis | Female | Antineoplastic Agents - pharmacology | Neoplasm Proteins - genetics | Nuclear Proteins - genetics | Cell Line, Tumor - metabolism | Melanoma - chemistry | Proto-Oncogene Proteins c-mdm2 - biosynthesis | Proto-Oncogene Proteins - antagonists & inhibitors | Tumor Stem Cell Assay | Membrane Proteins - genetics | Neoplasm Proteins - biosynthesis | Melanoma, Experimental - etiology | Mice, Inbred C57BL | Mice, Transgenic | Proto-Oncogene Proteins - genetics | Melanoma - pathology | Melanoma - secondary | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | Melanoma, Experimental - genetics | GTP Phosphohydrolases - genetics | Keratinocytes - metabolism | Mice, Nude | Nuclear Proteins - antagonists & inhibitors | Proto-Oncogene Proteins - physiology | Signal Transduction - physiology | Mice | Nuclear Proteins - physiology | Drug Resistance, Neoplasm - physiology | Drug Resistance, Neoplasm - drug effects | Care and treatment | Gene mutations | Melanoma | Diagnosis | Research | Gene expression | Identification and classification | Skin cancer | Proteins | Cell growth | Mutation | Cell cycle
Journal Article
Molecular Cell, ISSN 1097-2765, 09/2010, Volume 39, Issue 6, pp. 963 - 974
The melanoma antigen (MAGE) family consists of more than 60 genes, many of which are cancer-testis antigens that are highly expressed in cancer and play a... 
NECDIN GENE | EMERGING ROLES | MELANOMA | KAP1 | CANCER/TESTIS ANTIGENS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MDM2 INTERACTION | HOMOLOGOUS RECOMBINATION | CANCER-IMMUNOTHERAPY | CELL-LINES | EXPRESSION | CELL BIOLOGY | Melanoma-Specific Antigens - chemistry | Protein Interaction Domains and Motifs - physiology | Humans | Crystallography, X-Ray | Cytoplasm - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Neoplasm Proteins - metabolism | RING Finger Domains | Tripartite Motif-Containing Protein 28 | Ubiquitination | Cell Nucleus - metabolism | Transfection | Protein Structure, Quaternary | Antigens, Neoplasm - metabolism | Carrier Proteins - chemistry | Neoplasm Proteins - genetics | Intracellular Signaling Peptides and Proteins - genetics | Repressor Proteins - metabolism | Recombinant Proteins - metabolism | Antigens, Neoplasm - genetics | Cell Line | Biocatalysis | Tumor Suppressor Protein p53 - metabolism | Ubiquitin-Protein Ligases - metabolism | Models, Molecular | Recombinant Proteins - chemistry | Repressor Proteins - genetics | Recombinant Proteins - genetics | Ubiquitin-Protein Ligases - chemistry | Carrier Proteins - genetics | Carrier Proteins - metabolism | Intracellular Signaling Peptides and Proteins - chemistry | Melanoma-Specific Antigens - metabolism | Cell Line, Tumor | Ubiquitin-Protein Ligases - genetics | Melanoma-Specific Antigens - genetics | Protein Binding - physiology | Ubiquitin | Antigens | Ligases | Crystals | Melanoma | Structure | Tumor proteins | Protein binding
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 03/2016, Volume 291, Issue 13, pp. 6714 - 6722
The transcriptional coactivators CREB-binding protein (CBP) and p300 undergo a particularly rich set of interactions with disordered and partly ordered... 
ACTIVATION DOMAIN | UNSTRUCTURED PROTEINS | viral oncoprotein | intrinsically disordered protein | coupled folding and binding | intrinsically disordered region | BIOCHEMISTRY & MOLECULAR BIOLOGY | structure-function | STAT transcription factor | C-MYB | transcriptional coactivator | VIRAL-PROTEINS | transcriptional activation | P53 TRANSACTIVATION DOMAIN | COMPLEX-FORMATION | cAMP response element-binding protein (CREB) | hypoxia-inducible factor (HIF) | IDP | STRUCTURAL BASIS | IDR | KIX DOMAIN | TAZ2 DOMAIN | PEPTIDE MOTIFS | protein-protein interaction | Humans | E1A-Associated p300 Protein - genetics | STAT Transcription Factors - metabolism | CREB-Binding Protein - chemistry | NF-kappa B - metabolism | E1A-Associated p300 Protein - metabolism | NF-kappa B - chemistry | Viral Proteins - metabolism | Tumor Suppressor Protein p53 - genetics | CREB-Binding Protein - genetics | CREB-Binding Protein - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - chemistry | Transcription, Genetic | Protein Interaction Domains and Motifs | Protein Structure, Secondary | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Viral Proteins - chemistry | E1A-Associated p300 Protein - chemistry | Tumor Suppressor Protein p53 - metabolism | Models, Molecular | Viral Proteins - genetics | Intrinsically Disordered Proteins - genetics | Protein Folding | STAT Transcription Factors - genetics | NF-kappa B - genetics | Intrinsically Disordered Proteins - chemistry | Protein Binding | STAT Transcription Factors - chemistry | Tumor Suppressor Protein p53 - chemistry | Intrinsically Disordered Proteins - metabolism | Minireviews
Journal Article
Nature, ISSN 0028-0836, 08/2010, Volume 466, Issue 7307, pp. 765 - 768
Chronic myelogenous leukaemia (CML) can progress from a slow growing chronic phase to an aggressive blast crisis phase, but the molecular basis of this... 
CHRONIC MYELOGENOUS LEUKEMIA | MURINE MODEL | STEM-CELLS | TRANSLATIONAL REPRESSION | RNA | BINDING PROTEIN MUSASHI-1 | MULTIDISCIPLINARY SCIENCES | BCR-ABL | GENE-EXPRESSION | NUMB | CML BLAST CRISIS | RNA-Binding Proteins - genetics | Up-Regulation | Oncogene Proteins, Fusion - metabolism | Prognosis | Homeodomain Proteins - metabolism | Humans | Gene Expression Regulation, Neoplastic | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Nuclear Pore Complex Proteins - genetics | Cell Differentiation - genetics | RNA-Binding Proteins - biosynthesis | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Nerve Tissue Proteins - biosynthesis | Membrane Proteins - metabolism | Blast Crisis - pathology | Signal Transduction | Membrane Proteins - genetics | Nuclear Pore Complex Proteins - metabolism | Mice, Inbred C57BL | Tumor Suppressor Protein p53 - metabolism | Receptor, Notch1 - metabolism | Nerve Tissue Proteins - genetics | Disease Progression | Homeodomain Proteins - genetics | Nerve Tissue Proteins - metabolism | Fusion Proteins, bcr-abl - genetics | Membrane Proteins - biosynthesis | Animals | Oncogene Proteins, Fusion - genetics | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Blast Crisis - genetics | Mice | Blast Crisis - metabolism | Fusion Proteins, bcr-abl - metabolism | RNA-Binding Proteins - metabolism | Myelocytic leukemia | Molecular genetics | Physiological aspects | Development and progression | Nonlymphoid leukemia | Cellular signal transduction | Genetic aspects | Research | Genetic regulation | Gene expression | Medical research | Stem cells | Chronic illnesses
Journal Article