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Nature, ISSN 0028-0836, 2013, Volume 499, Issue 7456, pp. 50 - 54
53BP1 (also called TP53BP1) is a chromatin-associated factor that promotes immunoglobulin class switching and DNA double-strand-break (DSB) repair by... 
CRB2 | RECRUITMENT | FISSION YEAST | METHYLATION | CHROMATIN | DEPENDENT RESPONSE | RESECTION | MULTIDISCIPLINARY SCIENCES | SITES | DOUBLE-STRAND BREAKS | CLASS-SWITCH RECOMBINATION | Schizosaccharomyces pombe Proteins - chemistry | Histones - chemistry | Nucleosomes - chemistry | Humans | Ubiquitin - metabolism | Molecular Sequence Data | Male | Intracellular Signaling Peptides and Proteins - metabolism | DNA Breaks, Double-Stranded | DNA-Binding Proteins - deficiency | Cell Cycle Proteins - chemistry | Intracellular Signaling Peptides and Proteins - deficiency | Ubiquitination | Schizosaccharomyces pombe Proteins - metabolism | Female | Lysine - metabolism | Intracellular Signaling Peptides and Proteins - genetics | Schizosaccharomyces | Protein Structure, Tertiary | Amino Acid Sequence | Cell Line | Signal Transduction | Cell Cycle Proteins - metabolism | Nucleosomes - metabolism | Mutant Proteins - metabolism | Nuclear Proteins - metabolism | DNA-Binding Proteins - genetics | Nuclear Proteins - chemistry | DNA-Binding Proteins - chemistry | Chromosomal Proteins, Non-Histone - deficiency | Amino Acid Motifs | Chromosomal Proteins, Non-Histone - genetics | Animals | Intracellular Signaling Peptides and Proteins - chemistry | Mutant Proteins - chemistry | Protein Binding | Mice | DNA Damage | Histones - metabolism | Tumor Suppressor p53-Binding Protein 1 | Chromosomal Proteins, Non-Histone - chemistry | Ubiquitin | Research | Properties | DNA repair | DNA damage | Proteins | DNA methylation | Mutation | Experiments | Recruitment | Index Medicus
Journal Article
EMBO reports, ISSN 1469-221X, 01/2010, Volume 11, Issue 1, pp. 45 - 51
Autophagy is the cellular homeostatic pathway that delivers large cytosolic materials for degradation in the lysosome. Recent evidence indicates that autophagy... 
mitophagy | Nix | LC3 | GABARAP | selective autophagy | Selective autophagy | Mitophagy | APOPTOSIS | PROTEIN | RETICULOCYTE MATURATION | UBIQUITIN | BNIP3 | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL-DEATH | CELL BIOLOGY | STRUCTURAL BASIS | DEGRADATION | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Humans | Cercopithecus aethiops | Molecular Sequence Data | Substrate Specificity | Autophagy - physiology | Mitochondrial Proteins - genetics | Proto-Oncogene Proteins - chemistry | Mitochondrial Proteins - metabolism | Tumor Suppressor Proteins - chemistry | Tumor Suppressor Proteins - genetics | Membrane Proteins - metabolism | Binding Sites | Proto-Oncogene Proteins - metabolism | Amino Acid Sequence | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Cells, Cultured | Ubiquitin-Protein Ligases - metabolism | Proto-Oncogene Proteins - genetics | Mitochondria - metabolism | Saccharomyces cerevisiae Proteins - genetics | Blotting, Western | Amino Acid Motifs | Autophagy-Related Protein 8 Family | Animals | Membrane Proteins - chemistry | Reticulocytes - cytology | Mitochondrial Proteins - chemistry | Saccharomyces cerevisiae Proteins - metabolism | Protein Binding | Mice | Receptors, GABA-A - metabolism | COS Cells | Proteins | Mitochondria | Cellular biology | Cytoplasm | Index Medicus | Scientific Report
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 | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 03/2010, Volume 464, Issue 7287, pp. 431 - 435
Activating mutations in KRAS and BRAF are found in more than 30% of all human tumours and 40% of melanoma, respectively, thus targeting this pathway could have... 
SELECTIVE INHIBITOR | POTENT | EFFICACY | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | IN-VIVO | C-RAF | HETERODIMERIZATION | B-RAF | PROTEIN-KINASE KINASE | CANCER | Neoplasms - metabolism | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Diphenylamine - pharmacology | raf Kinases - antagonists & inhibitors | Humans | Protein Multimerization | ras Proteins - metabolism | Protein Transport - drug effects | Extracellular Signal-Regulated MAP Kinases - metabolism | raf Kinases - metabolism | Diphenylamine - analogs & derivatives | Mitogen-Activated Protein Kinase Kinases - metabolism | Adenosine Triphosphate - metabolism | Indoles - pharmacology | Benzamides - pharmacology | Cell Membrane - metabolism | raf Kinases - genetics | Cell Membrane - drug effects | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Pyrazoles - pharmacology | Protein Structure, Tertiary | Proto-Oncogene Proteins - metabolism | Cell Line | Indenes - pharmacology | raf Kinases - chemistry | Proto-Oncogene Proteins c-raf - genetics | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Neoplasms - enzymology | Proto-Oncogene Proteins - genetics | Enzyme Activation - drug effects | Sulfonamides - pharmacology | Proto-Oncogene Proteins c-raf - metabolism | Neoplasms - drug therapy | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | MAP Kinase Signaling System - drug effects | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Proto-Oncogene Proteins c-raf - deficiency | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Neoplasms - pathology | Ras genes | Growth | Physiological aspects | Cellular signal transduction | Genetic aspects | Research | Mitogen-activated protein kinases | Competition | Clinical trials | Enzymes | Kinases | Index Medicus | Proteins | Cellular | Inhibitors | Pathways | Tumours | Signalling | Dimerization
Journal Article
Molecular and Cellular Biology, ISSN 0270-7306, 04/2008, Volume 28, Issue 7, pp. 2426 - 2436
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... 
INACTIVATION | APOPTOSIS | PROTEIN | SIGNALING PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | YAP | SIZE-CONTROL | DIFFERENTIATION | DROSOPHILA | TUMOR-SUPPRESSOR PATHWAY | CELL BIOLOGY | 14-3-3 Proteins - physiology | Phosphorylation | Transferases (Other Substituted Phosphate Groups) - genetics | Humans | Receptor Protein-Tyrosine Kinases - physiology | Recombinant Fusion Proteins - physiology | Transferases (Other Substituted Phosphate Groups) - physiology | Mesoderm - cytology | Drosophila Proteins - physiology | Cell Transdifferentiation - physiology | Membrane Proteins - physiology | Cell Division | c-Mer Tyrosine Kinase | Cell Cycle Proteins - genetics | Conserved Sequence | Transcription, Genetic | Epithelial Cells - cytology | Proteins - physiology | Nerve Tissue Proteins - physiology | Transcription Factors - physiology | Membrane Proteins - genetics | Protein-Serine-Threonine Kinases - physiology | Protein-Serine-Threonine Kinases - genetics | Proto-Oncogene Proteins - genetics | Transcription Factors - genetics | Nerve Tissue Proteins - genetics | Protein Processing, Post-Translational - physiology | Amino Acid Motifs | Proteins - genetics | Receptor Protein-Tyrosine Kinases - genetics | Cell Transformation, Neoplastic | Proto-Oncogene Proteins - physiology | Cell Line, Tumor | Nuclear Proteins - physiology | Drosophila Proteins - genetics | Cell Cycle Proteins - physiology | Cell Movement | Index Medicus
Journal Article
Cell, ISSN 0092-8674, 2007, Volume 129, Issue 7, pp. 1415 - 1426
Protein kinases control cellular decision processes by phosphorylating specific substrates. Thousands of in vivo phosphorylation sites have been identified,... 
CELLBIO | ACTIVATION | DNA-DAMAGE RESPONSE | 53BP1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | KINASE | SPECTROMETRY-BASED PROTEOMICS | ATM | EUKARYOTIC PROTEINS | PROTEIN-PHOSPHORYLATION | MASS-SPECTROMETRY | SIGNALING NETWORKS | CELL BIOLOGY | Protein Kinases - metabolism | Phosphorylation | Protein Kinases - genetics | Humans | DNA Repair Enzymes - genetics | Intracellular Signaling Peptides and Proteins - metabolism | Phosphoproteins - metabolism | CDC2 Protein Kinase - metabolism | DNA-Binding Proteins - metabolism | Tumor Suppressor Proteins - genetics | DNA Repair Enzymes - metabolism | Cell Cycle Proteins - genetics | DNA Damage - genetics | Proteomics - methods | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Repressor Proteins - metabolism | CDC2 Protein Kinase - genetics | Computational Biology - methods | Tumor Suppressor Proteins - metabolism | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Repressor Proteins - genetics | Ataxia Telangiectasia Mutated Proteins | Binding Sites - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Glycogen Synthase Kinase 3 - metabolism | Transcription Factors - metabolism | Glycogen Synthase Kinase 3 - genetics | Signal Transduction - physiology | Software | Tumor Suppressor p53-Binding Protein 1 | Index Medicus
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 | Index Medicus
Journal Article
Science, ISSN 0036-8075, 12/2010, Volume 330, Issue 6009, pp. 1390 - 1393
Although the proteins BAX and BAK are required for initiation of apoptosis at the mitochondria, how BAX and BAK are activated remains unsettled. We provide in... 
T lymphocytes | Mitochondria | Cytokines | Thymocytes | Neurons | Cell death | REPORTS | Cytochromes | Mice | Potassium | Apoptosis | NEURONAL APOPTOSIS | CYTOCHROME-C | MITOCHONDRIAL APOPTOSIS | MECHANISM | MULTIDISCIPLINARY SCIENCES | BH3 DOMAINS | RELEASE | JNK PATHWAY | PROTEINS | BCL-2 FAMILY-MEMBERS | MEMBRANE PERMEABILIZATION | BH3 Interacting Domain Death Agonist Protein - deficiency | T-Lymphocytes - physiology | bcl-2-Associated X Protein - chemistry | Protein Multimerization | Stress, Physiological | bcl-2 Homologous Antagonist-Killer Protein - genetics | BH3 Interacting Domain Death Agonist Protein - genetics | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Membrane Proteins - deficiency | Caspases - metabolism | Bcl-2-Like Protein 11 | Apoptosis Regulatory Proteins - deficiency | Tumor Suppressor Proteins - deficiency | Tumor Suppressor Proteins - genetics | Neurons - physiology | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | BH3 Interacting Domain Death Agonist Protein - metabolism | bcl-2-Associated X Protein - genetics | Proto-Oncogene Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Cytochromes c - metabolism | Cells, Cultured | bcl-2-Associated X Protein - metabolism | Proto-Oncogene Proteins - genetics | Mitochondria - metabolism | Permeability | Proto-Oncogene Proteins - deficiency | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Animals | Models, Biological | Cerebellum - cytology | Intracellular Membranes - metabolism | bcl-2 Homologous Antagonist-Killer Protein - chemistry | Protein research | Genetic aspects | Mitochondrial DNA | Biochemical genetics | Research | Properties | Methods | Index Medicus
Journal Article