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Journal Article
Nature Medicine, ISSN 1078-8956, 09/2017, Volume 23, Issue 9, pp. 1055 - 1062
Bromodomain and extraterminal domain (BET) protein inhibitors are emerging as promising anticancer therapies. The gene encoding the E3 ubiquitin ligase... 
SELECTIVE-INHIBITION | TARGET | MEDICINE, RESEARCH & EXPERIMENTAL | ANDROGEN RECEPTOR | STEM-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | ACUTE MYELOID-LEUKEMIA | ENHANCERS | CELL BIOLOGY | RNA-SEQ | BROMODOMAIN INHIBITION | MUTATIONS | BRD4 | Prostatic Neoplasms - metabolism | Immunoprecipitation | TOR Serine-Threonine Kinases - metabolism | Humans | Drug Resistance, Neoplasm | Male | Gene Expression Profiling | Molecular Targeted Therapy | Mechanistic Target of Rapamycin Complex 1 | Transcription Factors - drug effects | Multiprotein Complexes - metabolism | Prostatic Neoplasms - genetics | Proteasome Endopeptidase Complex - drug effects | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Nuclear Proteins - drug effects | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | TOR Serine-Threonine Kinases - drug effects | Multiprotein Complexes - drug effects | Prostatic Neoplasms - drug therapy | Protein-Serine-Threonine Kinases - metabolism | Repressor Proteins - metabolism | RNA-Binding Proteins - antagonists & inhibitors | Triazoles - therapeutic use | Cell Survival | Repressor Proteins - genetics | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Azepines - therapeutic use | RNA-Binding Proteins - drug effects | Azepines - pharmacology | Transcription Factors - metabolism | Triazoles - pharmacology | Nuclear Proteins - antagonists & inhibitors | Protein-Serine-Threonine Kinases - drug effects | Cell Line, Tumor | Cell Proliferation - drug effects | Mutation | RNA-Binding Proteins - metabolism | rac1 GTP-Binding Protein - metabolism | Proto-Oncogene Proteins c-akt - drug effects | rac1 GTP-Binding Protein - genetics | Gene mutations | Physiological aspects | Genetic aspects | Research | Drug resistance | Drug therapy | Prostate cancer | Ubiquitin | Inhibitor drugs | Stabilization | AKT protein | Activation | Biosynthesis | Degradation | Proteins | Ubiquitination | Transcription activation | Ubiquitin-protein ligase | Binding | Rac1 protein | Tumor cell lines | Gene expression | Cholesterol | Mutants | Inhibitors | Proteasomes | Biomarkers | Bet protein | Prostate | Cancer | Guanosinetriphosphatase
Journal Article
Cell, ISSN 0092-8674, 05/2018, Volume 173, Issue 4, pp. 972 - 988.e23
Repair of damaged DNA is essential for maintaining genome integrity and for preventing genome-instability-associated diseases, such as cancer. By combining... 
DNA damage repair | proximity labeling | shieldin | proteomics | 53BP1 | PARP inhibitors | telomere maintenance | antibody class-switch recombination | NHEJ | BRCA1 | PATHWAYS | CELLS | RESECTION | DAMAGE-RESPONSE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CLASS-SWITCH RECOMBINATION | HOMOLOGOUS RECOMBINATION | DOUBLE-STRAND BREAK | TELOMERES | CELL BIOLOGY | Mad2 Proteins - metabolism | Humans | Ubiquitin-Protein Ligases - antagonists & inhibitors | DNA Breaks, Double-Stranded | Mad2 Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Telomere-Binding Proteins - genetics | RNA Interference | BRCA1 Protein - metabolism | Trans-Activators - genetics | Immunoglobulin Class Switching - drug effects | Nuclear Proteins - genetics | Telomere-Binding Proteins - metabolism | Tumor Suppressor p53-Binding Protein 1 - metabolism | DNA End-Joining Repair - drug effects | DNA-Binding Proteins - antagonists & inhibitors | Mutagenesis, Site-Directed | Tumor Suppressor p53-Binding Protein 1 - genetics | Ubiquitin-Protein Ligases - metabolism | Nuclear Proteins - metabolism | DNA-Binding Proteins - genetics | Telomere-Binding Proteins - antagonists & inhibitors | Tumor Suppressor p53-Binding Protein 1 - antagonists & inhibitors | BRCA1 Protein - genetics | Poly(ADP-ribose) Polymerase Inhibitors - pharmacology | BRCA1 Protein - antagonists & inhibitors | Mad2 Proteins - genetics | Cell Line, Tumor | Trans-Activators - metabolism | Ubiquitin-Protein Ligases - genetics | RNA, Small Interfering - metabolism | DNA damage | Genomics | Antibodies | Genomes | DNA repair | Proteins | Viral antibodies | Telomeres | Evolutionary biology | Analysis | DNA | Genetic research | Mass spectrometry
Journal Article
Journal of the National Cancer Institute, ISSN 0027-8874, 04/2011, Volume 103, Issue 8, pp. 645 - 661
Background Ionizing radiation (IR) is effectively used in cancer therapy. However, in subsets of patients, a few radioresistant cancer cells survive and cause... 
STEM-CELLS | IN-VITRO | ONCOLOGY | TYROSINE KINASE | HGF | CELL INVASION | RECEPTOR | EPITHELIAL-MESENCHYMAL TRANSITIONS | NF-KAPPA-B | SCATTER-FACTOR | PROTOONCOGENE | Humans | Neoplasm Invasiveness - prevention & control | Radiation Tolerance | Receptors, Growth Factor - antagonists & inhibitors | NF-kappa B - metabolism | RNA, Messenger - metabolism | NF-kappa B - radiation effects | Receptors, Growth Factor - genetics | Proto-Oncogene Proteins c-met - radiation effects | Signal Transduction - radiation effects | Protein-Serine-Threonine Kinases - metabolism | Radiation, Ionizing | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - radiation effects | Proto-Oncogene Proteins c-met - antagonists & inhibitors | Cell Cycle Proteins - metabolism | Cell Cycle Proteins - radiation effects | Receptors, Growth Factor - radiation effects | Proto-Oncogene Proteins c-met - drug effects | Ataxia Telangiectasia Mutated Proteins | Phosphorylation - radiation effects | Cell Line, Tumor | Mice | RNA, Small Interfering | Tumor Suppressor Proteins - radiation effects | Receptors, Growth Factor - metabolism | Neoplasms - metabolism | Proto-Oncogene Proteins c-met - metabolism | Apoptosis - radiation effects | Up-Regulation - radiation effects | Transcription, Genetic - radiation effects | Transplantation, Heterologous | Sulfones - pharmacology | DNA-Binding Proteins - metabolism | Chromatin Immunoprecipitation | Protein-Serine-Threonine Kinases - radiation effects | Tumor Suppressor Proteins - genetics | Polymerase Chain Reaction | Cell Cycle Proteins - genetics | Indoles - pharmacology | Neoplasms - radiotherapy | Gene Expression Regulation, Neoplastic - drug effects | In Situ Nick-End Labeling | Enzyme-Linked Immunosorbent Assay | Radiation-Sensitizing Agents - pharmacology | Gene Silencing | Protein-Serine-Threonine Kinases - genetics | DNA-Binding Proteins - genetics | Cell Survival - radiation effects | Cell Movement - radiation effects | Proto-Oncogene Proteins c-met - genetics | Blotting, Northern | Animals | NF-kappa B - genetics | Protein Kinase Inhibitors - pharmacology | Neoplasms - pathology | Receptors, Growth Factor - drug effects | DNA Damage - radiation effects | Mitogen-Activated Protein Kinases - metabolism | Ionizing radiation | Physiological aspects | Genetic aspects | Cancer invasiveness | Research | Gene expression | Radiotherapy | Health aspects
Journal Article
Nature Structural & Molecular Biology, ISSN 1545-9993, 10/2010, Volume 17, Issue 10, pp. 1247 - 1254
Inherited mutations in human PALB2 are associated with a predisposition to breast and pancreatic cancers. PALB2's tumor-suppressing effect is thought to be... 
POLY(ADP-RIBOSE) POLYMERASE | COMPLEX | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOUBLE-STRAND BREAKS | HISTONE H2AX | FANCONI-ANEMIA | CELL BIOLOGY | RAD51 | BIOPHYSICS | IN-VIVO | SUSCEPTIBILITY GENE | D-LOOP FORMATION | DNA-REPAIR | Recombination, Genetic - physiology | DNA, Neoplasm - metabolism | Humans | Neoplasm Proteins - physiology | DNA Repair - physiology | Molecular Sequence Data | Structure-Activity Relationship | DNA Breaks, Double-Stranded | BRCA2 Protein - physiology | Breast Neoplasms - metabolism | Base Sequence | Tumor Suppressor Proteins - chemistry | Tumor Suppressor Proteins - genetics | Female | Protein Interaction Domains and Motifs | Nuclear Proteins - genetics | Nucleic Acid Conformation | Fanconi Anemia Complementation Group N Protein | Peptide Fragments - metabolism | Neoplasm Proteins - chemistry | Nuclear Proteins - chemistry | Poly(ADP-ribose) Polymerase Inhibitors | Protein Interaction Mapping | Tumor Suppressor Proteins - physiology | Peptide Fragments - chemistry | Apoptosis Regulatory Proteins | Models, Biological | Rad51 Recombinase - chemistry | Rad51 Recombinase - physiology | BRCA2 Protein - chemistry | Nuclear Proteins - physiology | Poly (ADP-Ribose) Polymerase-1 | Breast cancer | Genetic aspects | Research | BRCA mutations | Ovarian cancer | Proteins | Mutation | Molecular biology | Prostate cancer | homologous recombination | BRCA2 | PALB2
Journal Article
Molecular Cell, ISSN 1097-2765, 08/2017, Volume 67, Issue 3, pp. 387 - 399.e5
The DNA-mediated innate immune response underpins anti-microbial defenses and certain autoimmune diseases. Here we used immunoprecipitation, mass spectrometry,... 
HEXIM1 | DNA-PK | innate immune response | herpesvirus | paraspeckles | cGAS | NEAT1 | interferon stimulatory DNA | DEFENSE | PROTEIN | INHIBITION | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | SENSOR | POLYMERASE-II | 7SK RNA | BINDING | GMP-AMP SYNTHASE | P-TEFB | CELL BIOLOGY | Human Umbilical Vein Endothelial Cells - metabolism | Humans | Octamer Transcription Factors - immunology | Intracellular Signaling Peptides and Proteins - metabolism | Herpesvirus 8, Human - immunology | RNA, Long Noncoding - immunology | PTB-Associated Splicing Factor - genetics | RNA Interference | Calcium-Binding Proteins - immunology | Octamer Transcription Factors - genetics | Nucleotidyltransferases - metabolism | Intracellular Signaling Peptides and Proteins - genetics | Signal Transduction | Membrane Proteins - genetics | RNA-Binding Proteins - immunology | PTB-Associated Splicing Factor - metabolism | Nuclear Matrix-Associated Proteins - metabolism | PTB-Associated Splicing Factor - immunology | DNA - metabolism | Host-Pathogen Interactions | Nuclear Matrix-Associated Proteins - genetics | HeLa Cells | RNA-Binding Proteins - metabolism | Calcium-Binding Proteins - genetics | RNA-Binding Proteins - genetics | Multiprotein Complexes | Human Umbilical Vein Endothelial Cells - immunology | Intracellular Signaling Peptides and Proteins - immunology | Human Umbilical Vein Endothelial Cells - virology | Interferon Regulatory Factor-3 - genetics | Ku Autoantigen - genetics | Transfection | HEK293 Cells | Membrane Proteins - metabolism | Nuclear Proteins - genetics | Octamer Transcription Factors - metabolism | Interferon Regulatory Factor-3 - immunology | Calcium-Binding Proteins - metabolism | DNA - immunology | Nuclear Matrix-Associated Proteins - immunology | Ku Autoantigen - immunology | Membrane Proteins - immunology | Nuclear Proteins - metabolism | Ku Autoantigen - metabolism | RNA, Long Noncoding - genetics | Immunity, Innate | Nuclear Proteins - immunology | DNA - genetics | Interferon Regulatory Factor-3 - metabolism | Nucleotidyltransferases - genetics | Protein Binding | Nucleotidyltransferases - immunology | RNA, Long Noncoding - metabolism | RNA sequencing | Immune response | RNA | DNA | Genetic research | Interferon | Biological response modifiers | Mass spectrometry | Human Umbilical Vein Endothelial Cells | Nuclear Matrix-Associated Proteins | Herpesvirus 8, Human | RNA-Binding Proteins | Life Sciences | Interferon Regulatory Factor-3 | Genetics | Calcium-Binding Proteins | Intracellular Signaling Peptides and Proteins | PTB-Associated Splicing Factor | Nuclear Proteins | Membrane Proteins | Nucleotidyltransferases | Ku Autoantigen | Octamer Transcription Factors | RNA, Long Noncoding
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 05/2012, Volume 18, Issue 9, pp. 2502 - 2514
Purpose: The clinical use of BRAF inhibitors is being hampered by the acquisition of drug resistance. This study shows the potential therapeutic use of the... 
BREAST-CANCER | MULTIPLE-MYELOMA | APOPTOSIS | PHASE-II TRIAL | TANESPIMYCIN 17-AAG | TRASTUZUMAB | ONCOLOGY | BIM | ACQUIRED-RESISTANCE | MELANOMA-CELLS | POTENTIAL MECHANISM | Prospective Studies | Apoptosis - drug effects | Humans | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Immunoenzyme Techniques | Forkhead Transcription Factors - metabolism | Colony-Forming Units Assay | Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization | Phthalic Acids - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Real-Time Polymerase Chain Reaction | Proto-Oncogene Proteins B-raf - metabolism | Membrane Proteins - genetics | Melanoma - pathology | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Apoptosis Regulatory Proteins - metabolism | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Indoles - adverse effects | Membrane Proteins - antagonists & inhibitors | Signal Transduction - drug effects | HSP90 Heat-Shock Proteins - antagonists & inhibitors | Cell Line, Tumor | HSP90 Heat-Shock Proteins - metabolism | Mice | Mice, Inbred BALB C | Forkhead Box Protein O3 | Azabicyclo Compounds - pharmacology | Phosphatidylinositol 3-Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - genetics | Proto-Oncogene Proteins c-akt - genetics | Proto-Oncogene Proteins c-bcl-2 - metabolism | Flow Cytometry | Bcl-2-Like Protein 11 | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | Forkhead Transcription Factors - antagonists & inhibitors | Melanoma - metabolism | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | RNA, Messenger - genetics | Proto-Oncogene Proteins - genetics | Forkhead Transcription Factors - genetics | Phosphatidylinositol 3-Kinases - genetics | Animals | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Myeloid Cell Leukemia Sequence 1 Protein | Apoptosis Regulatory Proteins - antagonists & inhibitors | Fluorescent Antibody Technique | Sulfonamides - adverse effects | Proto-Oncogene Proteins c-bcl-2 - antagonists & inhibitors | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Proto-Oncogene Proteins c-bcl-2 - genetics | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Drug Resistance, Neoplasm - drug effects
Journal Article
Science, ISSN 0036-8075, 5/2012, Volume 336, Issue 6081, pp. 593 - 597
The telomere end-protection problem is defined by the aggregate of DNA damage signaling and repair pathways that require repression at telomeres. To define the... 
Telomeres | Yeasts | Quantification | Lymphocytes | DNA | DNA damage | REPORTS | Cell cycle | Ataxia telangiectasia | Repression | Chromosomes | JOINING PATHWAY | POT1 PROTEINS | MAMMALIAN TELOMERES | SGS1 | MULTIDISCIPLINARY SCIENCES | DYSFUNCTIONAL TELOMERES | DOUBLE-STRAND BREAKS | HOMOLOGOUS RECOMBINATION | NHEJ | YEAST KU | Telomere - ultrastructure | Antigens, Nuclear - metabolism | Telomeric Repeat Binding Protein 1 - genetics | Telomeric Repeat Binding Protein 1 - metabolism | Homologous Recombination | DNA Breaks, Double-Stranded | DNA Ligases - metabolism | DNA-Binding Proteins - metabolism | Poly-ADP-Ribose Binding Proteins | Telomere-Binding Proteins - genetics | DNA End-Joining Repair | Telomere - metabolism | Telomere-Binding Proteins - metabolism | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | Chromosomal Proteins, Non-Histone - metabolism | Signal Transduction | Cell Cycle Proteins - metabolism | Cells, Cultured | Ataxia Telangiectasia Mutated Proteins | Xenopus Proteins | DNA-Binding Proteins - genetics | Telomere Homeostasis | Mice, Knockout | Poly(ADP-ribose) Polymerases - metabolism | Animals | Antigens, Nuclear - genetics | Cell Cycle | Ku Autoantigen | DNA Repair | DNA Ligase ATP | Telomeric Repeat Binding Protein 2 - metabolism | Mice | Poly (ADP-Ribose) Polymerase-1 | Telomeric Repeat Binding Protein 2 - genetics | Tumor Suppressor p53-Binding Protein 1 | Proteins | Physiological aspects | Research | Health aspects | DNA repair | Telomerase
Journal Article
Molecular Cell, ISSN 1097-2765, 10/2015, Volume 60, Issue 2, pp. 231 - 241
Phase-separated states of proteins underlie ribonucleoprotein (RNP) granules and nuclear RNA-binding protein assemblies that may nucleate protein inclusions... 
CELL-FREE FORMATION | PROTEIN | PHOSPHORYLATION | PRION-LIKE DOMAINS | PHASE-TRANSITIONS | TDP-43 | BIOCHEMISTRY & MOLECULAR BIOLOGY | ALS | FUS/TLS | ARGININE METHYLATION | ALPHA-SYNUCLEIN | CELL BIOLOGY | RNA-Binding Proteins - genetics | Humans | Molecular Sequence Data | RNA Polymerase II - metabolism | Cytoplasmic Granules - chemistry | Phase Transition | RNA-Binding Protein FUS - chemistry | Molecular Mimicry | Cytoplasmic Granules - metabolism | Escherichia coli - metabolism | Binding Sites | RNA Polymerase II - chemistry | RNA - metabolism | Protein Structure, Tertiary | Recombinant Proteins - metabolism | Prions - metabolism | Gene Expression | Rheology | RNA-Binding Proteins - chemistry | RNA-Binding Protein FUS - genetics | Recombinant Proteins - chemistry | RNA-Binding Protein FUS - metabolism | Recombinant Proteins - genetics | Prions - chemistry | RNA - chemistry | Intrinsically Disordered Proteins - genetics | Amino Acid Motifs | Escherichia coli - genetics | Intrinsically Disordered Proteins - chemistry | Protein Binding | RNA Polymerase II - genetics | RNA-Binding Proteins - metabolism | Intrinsically Disordered Proteins - metabolism | Proteins | Nervous system diseases | Sarcoma | RNA | Physiological aspects | Fluorescence | Nuclear magnetic resonance spectroscopy | Molecular biology | Fluorescence microscopy | Cells | Protein binding | Analysis
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 10/2013, Volume 110, Issue 43, pp. 17368 - 17373
Large tumor suppressor (LATS)1/2 protein kinases transmit Hippo signaling in response to intercellular contacts and serum levels to limit cell growth via the... 
Cell growth | Phosphorylation | Starvation | Epithelial cells | Cell lines | Actins | Gene expression regulation | Breast cancer | Cellular immunity | Endothelial cells | Itch | Growth control | YES-ASSOCIATED PROTEIN | MIGRATION | REGULATOR | COMPLEX | DOMAIN | ACTIN | MULTIDISCIPLINARY SCIENCES | growth control | breast cancer | HIPPO PATHWAY REGULATION | FAMILY PROTEINS | Transcription, Genetic - drug effects | Humans | Phosphoproteins - metabolism | Intercellular Signaling Peptides and Proteins - metabolism | MCF-7 Cells | RNA Interference | Tumor Suppressor Proteins - genetics | HEK293 Cells | Membrane Proteins - metabolism | Phosphorylation - drug effects | Culture Media, Serum-Free - pharmacology | Protein-Serine-Threonine Kinases - metabolism | Repressor Proteins - metabolism | 14-3-3 Proteins - genetics | Amino Acid Sequence | Cell Line | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Intercellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - genetics | Ubiquitin-Protein Ligases - metabolism | Repressor Proteins - genetics | Serine - genetics | Binding Sites - genetics | Phosphoproteins - genetics | Reverse Transcriptase Polymerase Chain Reaction | Serine - metabolism | Blotting, Western | 14-3-3 Proteins - metabolism | Microscopy, Confocal | Animals | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Protein Binding | Cell Proliferation - drug effects | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Ubiquitin-Protein Ligases - genetics | Cell proliferation | Physiological aspects | Genetic transcription | Research | Protein kinases | Biological Sciences
Journal Article