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Nature cell biology, ISSN 1476-4679, 2018, Volume 20, Issue 8, pp. 954 - 965
BRCA1 deficiencies cause breast, ovarian, prostate and other cancers, and render tumours hypersensitive to poly(ADP-ribose) polymerase (PARP) inhibitors. To... 
PATHWAY CHOICE | STRAND BREAK REPAIR | RESECTION | DAMAGE-RESPONSE | 53BP1 | CLASS-SWITCH RECOMBINATION | FANCONI-ANEMIA | DIFFERENTIAL EXPRESSION ANALYSIS | POLYMERASE-ZETA | TELOMERES | CELL BIOLOGY | Osteosarcoma - drug therapy | Mad2 Proteins - metabolism | Humans | Multiprotein Complexes | Ovarian Neoplasms - pathology | Bone Neoplasms - pathology | DNA Breaks, Double-Stranded | Bone Neoplasms - metabolism | Breast Neoplasms - metabolism | Dose-Response Relationship, Drug | Ovarian Neoplasms - genetics | Telomere-Binding Proteins - genetics | DNA End-Joining Repair | HEK293 Cells | Female | Bone Neoplasms - genetics | Ovarian Neoplasms - metabolism | Bone Neoplasms - drug therapy | BRCA1 Protein - deficiency | Telomere-Binding Proteins - metabolism | Ovarian Neoplasms - drug therapy | Osteosarcoma - metabolism | DNA-Binding Proteins | Tumor Suppressor p53-Binding Protein 1 - metabolism | Recombinational DNA Repair | Tumor Suppressor p53-Binding Protein 1 - genetics | Cisplatin - pharmacology | Breast Neoplasms - drug therapy | Proteins - genetics | Xenograft Model Antitumor Assays | BRCA1 Protein - genetics | Poly(ADP-ribose) Polymerase Inhibitors - pharmacology | Drug Resistance, Neoplasm - genetics | Animals | Breast Neoplasms - genetics | Proteins - metabolism | Breast Neoplasms - pathology | Mad2 Proteins - genetics | Cell Line, Tumor | Mice | Osteosarcoma - genetics | Cell Cycle Proteins | Osteosarcoma - pathology | Care and treatment | DNA | Cancer cells | Breast cancer | Genetic aspects | Research | Gene expression | Single-stranded DNA | DNA damage | Homologous recombination | Poly(ADP-ribose) | Homology | Genomes | Inactivation | Proteins | Ribose | Null cells | Deoxyribonucleic acid--DNA | BRCA2 protein | CRISPR | Deactivation | BRCA1 protein | Poly(ADP-ribose) polymerase | Adenosine diphosphate | Oligosaccharides | Double-strand break repair | Screens | Cisplatin | Polymerase | Inhibitors | Prostate | Viability | Tumors | Telomere-Binding Proteins / metabolism | Osteosarcoma / genetics | Telomere-Binding Proteins / genetics | BRCA1 Protein / genetics | Cellular Biology | Genetics | Proteins / genetics | Osteosarcoma / drug therapy | Ovarian Neoplasms / genetics | Mad2 Proteins / genetics | Proteins / metabolism | Breast Neoplasms / drug therapy | Breast Neoplasms / metabolism | Tumor Suppressor p53-Binding Protein 1 / genetics | BRCA1 Protein / deficiency | Ovarian Neoplasms / metabolism | Mad2 Proteins / metabolism | Breast Neoplasms / pathology | Bone Neoplasms / genetics | Ovarian Neoplasms / pathology | Bone Neoplasms / pathology | Life Sciences | Bone Neoplasms / drug therapy | Ovarian Neoplasms / drug therapy | Osteosarcoma / metabolism | Biochemistry, Molecular Biology | Breast Neoplasms / genetics | Drug Resistance, Neoplasm / genetics | Osteosarcoma / pathology | Bone Neoplasms / metabolism | Poly(ADP-ribose) Polymerase Inhibitors / pharmacology | Cisplatin / pharmacology | Molecular biology | Tumor Suppressor p53-Binding Protein 1 / metabolism | Cancer
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 01/2014, Volume 124, Issue 1, pp. 367 - 384
There is a considerable resurgence of interest in the role of aerobic glycolysis in cancer; however, increased glycolysis is frequently viewed as a consequence... 
MEDICINE, RESEARCH & EXPERIMENTAL | GENE-EXPRESSION SIGNATURE | SOLUBLE ADENYLYL-CYCLASE | VIRUS-TRANSFORMED CELLS | GLUCOSE-METABOLISM | PYRUVATE-KINASE M2 | EPIDERMAL-GROWTH-FACTOR | RECONSTITUTED BASEMENT-MEMBRANE | EXTRACELLULAR-MATRIX | HUMAN BREAST CELLS | MAMMARY EPITHELIAL-CELLS | Up-Regulation | Humans | Glucose Transporter Type 3 - metabolism | Acetylglucosamine - metabolism | Breast Neoplasms - metabolism | Receptor, Epidermal Growth Factor - metabolism | Guanine Nucleotide Exchange Factors - metabolism | Female | Membrane Proteins - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Telomere-Binding Proteins - metabolism | Oncogenes | Second Messenger Systems | Cell Line | Oxygen Consumption | Biosynthetic Pathways | Glycosylation | MAP Kinase Kinase Kinases - metabolism | Adenylyl Cyclases - metabolism | Cell Transformation, Neoplastic - metabolism | Integrin beta1 - metabolism | Phenotype | Carrier Proteins - metabolism | Thyroid Hormones - metabolism | Glucose - metabolism | Glycolysis | Breast Neoplasms - mortality | Protein Processing, Post-Translational | Complications and side effects | Care and treatment | Patient outcomes | Physiological aspects | Development and progression | Research | Carcinogenesis | Risk factors | Integrins | Medical research | Dehydrogenases | Metabolites | Cloning | Breast cancer | Glucose | Metabolism | Gene expression
Journal Article
Science (American Association for the Advancement of Science), ISSN 1095-9203, 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, 2013, Volume 49, Issue 1, pp. 172 - 185
The metabolism of glucose and glutamine, primary carbon sources utilized by mitochondria to generate energy and macromolecules for cell growth, is directly regulated by mTORC1... 
TARGET | RAPTOR | TEL2 | TUMOR-SUPPRESSOR COMPLEX | RAG GTPASES | PROTEIN-KINASE | STABILITY | BIOCHEMISTRY & MOLECULAR BIOLOGY | GROWTH | CELL-CYCLE PROGRESSION | NUTRIENT | CELL BIOLOGY | Glutamine - deficiency | Humans | Multiprotein Complexes | Protein Multimerization | Stress, Physiological | Breast Neoplasms - metabolism | Mechanistic Target of Rapamycin Complex 1 | Telomere-Binding Proteins - genetics | Ribosomal Protein S6 Kinases, 90-kDa - metabolism | Lysosomes - metabolism | Adenosine Triphosphate - metabolism | Adenylate Kinase - metabolism | Tumor Suppressor Proteins - genetics | Statistics, Nonparametric | Female | Telomere-Binding Proteins - metabolism | DNA Helicases - genetics | ATPases Associated with Diverse Cellular Activities | Tumor Suppressor Proteins - metabolism | Signal Transduction | Cells, Cultured | Citric Acid Cycle | Mice, Knockout | Protein Transport | Carrier Proteins - genetics | DNA Helicases - metabolism | Glucose - deficiency | Animals | Breast Neoplasms - genetics | Carrier Proteins - metabolism | Proteins - metabolism | Energy Metabolism | Monomeric GTP-Binding Proteins - metabolism | Protein Binding | Carcinoma - genetics | Mice | TOR Serine-Threonine Kinases | Carcinoma - metabolism | Proteins | Glucose metabolism | Physiological aspects | Stress (Physiology) | Mitochondrial DNA | Glucose | Cells | Dextrose | Glutamine
Journal Article
Journal Article
Nature (London), ISSN 1476-4687, 2007, Volume 449, Issue 7164, pp. 928 - 932
Journal Article
Nature (London), ISSN 1476-4687, 2011, Volume 470, Issue 7334, pp. 359 - 365
...) or telomerase RNA component (Terc) genes. Consistent with PGCs as master regulators of mitochondrial physiology and metabolism, telomere dysfunction is associated with impaired mitochondrial... 
STEM-CELLS | HOMEOSTASIS | BIOGENESIS | PGC-1-ALPHA | MULTIDISCIPLINARY SCIENCES | HEART-FAILURE | LEADS | MICE | CARCINOMA | DAMAGE | COACTIVATORS | Cell Proliferation | Reactive Oxygen Species - metabolism | Hematopoietic Stem Cells - pathology | DNA, Mitochondrial - analysis | Adenosine Triphosphate - biosynthesis | Tumor Suppressor Protein p53 - genetics | RNA - genetics | Telomerase - deficiency | Cardiomyopathies - physiopathology | Telomerase - genetics | Myocardium - metabolism | Telomere - metabolism | Gluconeogenesis | Telomere - genetics | Liver - metabolism | Tumor Suppressor Protein p53 - metabolism | Cardiomyopathies - pathology | Transcription Factors - antagonists & inhibitors | Hematopoietic Stem Cells - metabolism | Mitochondria - metabolism | Mitochondria - pathology | Tumor Suppressor Protein p53 - deficiency | Doxorubicin - toxicity | Aging - pathology | Myocardium - cytology | Transcription Factors - metabolism | Telomere - pathology | Animals | Cardiomyopathies - metabolism | Telomere - enzymology | Liver - cytology | Mice | Aging - metabolism | Cardiomyopathies - chemically induced | Telomeres | Mitochondria | Genetic aspects | Chemical properties | Abnormalities | Liver | Cell division | Mitochondrial DNA | Biosynthesis | Biology | DNA repair | Proteins | Studies | Aging | Telomerase | Binding sites | Apoptosis
Journal Article
Journal Article
Journal of Thoracic and Cardiovascular Surgery, The, ISSN 0022-5223, 2017, Volume 154, Issue 3, pp. 966 - 975.e4
Abstract Objective Idiopathic and postsurgical constrictive pericarditis is characterized by pericardial structural remodeling that involves fibrosis,... 
Cardiothoracic Surgery | senescence | constrictive pericarditis | pericardial interstitial cell | structural remodeling | FIBROSIS | SURGERY | CARDIAC & CARDIOVASCULAR SYSTEMS | MONOCYTE CHEMOATTRACTANT | DOWN-REGULATION | STELLATE CELLS | REPLICATIVE SENESCENCE | ENDOTHELIAL PROGENITOR CELLS | ADHESION | RESPIRATORY SYSTEM | CALCIFICATION | SMOOTH-MUSCLE-CELLS | TELOMERE LENGTH | Tumor Necrosis Factor-alpha - metabolism | Up-Regulation | Cell Proliferation | Humans | Collagen Type III - metabolism | Osteopontin - metabolism | RNA, Messenger - metabolism | Case-Control Studies | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Telomere Shortening | Collagen Type I - genetics | Cellular Senescence | beta-Galactosidase - metabolism | Cell Differentiation | Interleukin-6 - metabolism | Extracellular Matrix Proteins - metabolism | Calcium-Binding Proteins - metabolism | Pericarditis, Constrictive - pathology | Collagen Type I - metabolism | Down-Regulation | Cells, Cultured | Osteonectin - metabolism | Matrix Metalloproteinase 3 - metabolism | Collagen Type III - genetics | Fibronectins - metabolism | Pericardium - cytology | Tissue Inhibitor of Metalloproteinase-1 - genetics | Connective Tissue Growth Factor - genetics | Fibronectins - genetics | Matrix Metalloproteinase 1 - metabolism | Integrin-Binding Sialoprotein - metabolism | Connective Tissue Growth Factor - metabolism | Fibronectins | Enzymes | Telomeres | Interleukins | Collagen | Bone morphogenetic proteins | Gene expression
Journal Article