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1. Full Text Limiting replication stress during somatic cell reprogramming reduces genomic instability in induced pluripotent stem cells
by Ruiz, Sergio and Lopez-Contreras, Andres J and Gabut, Mathieu and Marion, Rosa M and Gutierrez-Martinez, Paula and Bua, Sabela and Ramirez, Oscar and Olalde, Iñigo and Rodrigo-Perez, Sara and Li, Han and Marques-Bonet, Tomas and Serrano, Manuel and Blasco, Maria A and Batada, Nizar N and Fernandez-Capetillo, Oscar
Nature Communications, ISSN 2041-1723, 08/2015, Volume 6, Issue 1, p. 8036
The generation of induced pluripotent stem cells (iPSC) from adult somatic cells is one of the most remarkable discoveries in recent decades. However, several... 
CODING MUTATIONS | CANCER DEVELOPMENT | CHK1 | INITIATION | MULTIDISCIPLINARY SCIENCES | COPY NUMBER | GENERATION | MODEL | ABERRATIONS | TELOMERE FRAGILITY | ATR | Protein Kinases - metabolism | Stress, Physiological - physiology | Cell Line | Nucleic Acid Hybridization | Protein Kinases - genetics | Induced Pluripotent Stem Cells - physiology | Fibroblasts - physiology | Humans | Cell Proliferation - physiology | Gene Expression Regulation - physiology | Genomic Instability - physiology | Mice, Transgenic | DNA - genetics | Point Mutation | Animals | Plasmids | Checkpoint Kinase 1 | Mice | Cellular Reprogramming - physiology | Citologia | Biologia molecular
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2. Full Text Replication stress and cancer: It takes two to tango
by Lecona, Emilio and Fernández-Capetillo, Oscar
Experimental Cell Research, ISSN 0014-4827, 11/2014, Volume 329, Issue 1, pp. 26 - 34
Problems arising during DNA replication require the activation of the ATR–CHK1 pathway to ensure the stabilization and repair of the forks, and to prevent the... 
Replication Stress | CHK1 | ATR | Cancer | RNA-POLYMERASE-II | HOLLIDAY JUNCTION RESOLUTION | ONCOGENE-INDUCED SENESCENCE | SELECTIVE CHK1 INHIBITOR | FANCONI-ANEMIA | DNA-REPLICATION | CELL BIOLOGY | GENOMIC INSTABILITY | ONCOLOGY | RIBONUCLEOTIDE REDUCTASE INHIBITOR | ATR PROTEIN-KINASE | ATAXIA-TELANGIECTASIA | Neoplasms - genetics | Signal Transduction | Gene Rearrangement | Humans | DNA Replication | Chromosomal Instability | Neoplasms - epidemiology | Chemotherapy | DNA replication | Genomics | Cellular biology | DNA repair | Stress
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3. Full Text Nuclear phosphoinositide 3-kinase β controls double-strand break DNA repair
by Amit Kumar and Oscar Fernadez-Capetillo and Ana C. Carrera and Tak Wah Mak
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 4/2010, Volume 107, Issue 16, pp. 7491 - 7496
Class I phosphoinositide 3-kinases are enzymes that generate 3-poly-phosphoinositides at the cell membrane following transmembrane receptor stimulation.... 
Chromatin | 3T3 cells | NIH 3T3 cells | Lasers | DNA damage | DNA | Cell cycle | Infrared radiation | Gene expression regulation | DNA repair | Genomic integrity | Cancer | P110-ALPHA | ACTIVATION | COMPLEX | CHROMATIN | MULTIDISCIPLINARY SCIENCES | genomic integrity | DAMAGE RESPONSE | SITES | EMBRYONIC LETHALITY | cancer | CHECKPOINT | ATM | MICE | Genomic Instability | NIH 3T3 Cells | Cell Cycle Proteins - metabolism | DNA Replication | Nuclear Proteins - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - genetics | Animals | Cell Nucleus - metabolism | Class I Phosphatidylinositol 3-Kinases | Models, Biological | DNA Repair | Gene Deletion | Protein Isoforms | Mice | DNA Damage | Neoplasms - pathology | Fibroblasts - metabolism | Biological Sciences
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4. Full Text Targeting ATR in cancer
by Lecona, Emilio and Fernandez-Capetillo, Oscar
Nature Reviews Cancer, ISSN 1474-175X, 09/2018, Volume 18, Issue 9, pp. 586 - 595
The chemical treatment of cancer started with the realization that DNA damaging agents such as mustard gas present notable antitumoural properties.... 
Genomic Instability | Nitroso Compounds - therapeutic use | Ataxia Telangiectasia Mutated Proteins - metabolism | Humans | Pyrazines - therapeutic use | Molecular Targeted Therapy | Neoplasms - drug therapy | Neoplasms - genetics | Oxazines - therapeutic use | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Sulfoxides - therapeutic use | Ataxia Telangiectasia Mutated Proteins - antagonists & inhibitors | Quinolines - therapeutic use | DNA Damage | Drug Development | Isoxazoles - therapeutic use | GENOMIC INSTABILITY | MCM PROTEINS | ONCOLOGY | DNA-DAMAGE RESPONSE | PROTEIN-KINASE | SYNTHETIC LETHALITY | HOMOLOGOUS RECOMBINATION | REPLICATION CHECKPOINT RESPONSE | ONCOGENE-INDUCED SENESCENCE | ATAXIA-TELANGIECTASIA | FORK PROGRESSION | Care and treatment | Oncology, Experimental | Genetic aspects | Research | Biological markers | Protein kinases | Cancer | Medical research | Stability | DNA damage | Genotoxicity | Clinical trials | Drug development | Kinases | Genomic instability | Anticancer properties | Proteins | Organic chemistry | Side effects | Chemical treatment | Mustard gas | Biomarkers | Ataxia | Ataxia telangiectasia mutated protein | Ataxia telangiectasia | Mustard | Damage | Deoxyribonucleic acid--DNA | Genotoxic chemicals
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5. Full Text A SUMO and ubiquitin code coordinates protein traffic at replication factories
: USP7 as a replication-associated SUMO DUB
by Lecona, Emilio and Fernandez-Capetillo, Oscar
BioEssays, ISSN 0265-9247, 12/2016, Volume 38, Issue 12, pp. 1209 - 1217
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6. Full Text Targeting ATR and Chk1 kinases for cancer treatment: A new model for new (and old) drugs
by Toledo, Luis I and Murga, Matilde and Fernandez-Capetillo, Oscar
Molecular Oncology, ISSN 1574-7891, 2011, Volume 5, Issue 4, pp. 368 - 373
Trying to kill cancer cells by generating DNA damage is by no means a new idea. Radiotherapy and genotoxic drugs are routinely used in cancer therapy. More... 
Cancer therapy | Chk1 | ATR | EARLY EMBRYONIC LETHALITY | CHROMOSOMAL FRAGMENTATION | DOUBLE-STRAND BREAKS | ADULT MICE | DEFICIENT MICE | GENOMIC INSTABILITY | DNA-DAMAGE CHECKPOINT | ONCOLOGY | REPLICATION FORK | SYNTHETIC LETHALITY | ATAXIA-TELANGIECTASIA | Protein Kinases - metabolism | Protein Kinases - genetics | Humans | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Ataxia Telangiectasia Mutated Proteins | DNA Breaks, Double-Stranded | Enzyme Inhibitors - therapeutic use | Tumor Suppressor Protein p53 - genetics | Neoplasms - drug therapy | Neoplasms - genetics | Cell Cycle Proteins - genetics | Checkpoint Kinase 1 | DNA Damage | Protein-Serine-Threonine Kinases - metabolism | Drugs | Care and treatment | Analysis | Aircraft industry | Tumor proteins | Drug therapy | Phosphotransferases | Cancer | Phosphorylation | p53 Protein | CHK1 protein | DNA damage | Genotoxicity | Radiation therapy | Kinases | Patients | Cancer therapies | Ataxia | Mutation | Deoxyribonucleic acid--DNA | Tumors | Apoptosis | Reviews | Review
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7. Full Text A SUMO and ubiquitin code coordinates protein traffic at replication factories
by Lecona, Emilio and Fernandez‐Capetillo, Oscar
BioEssays, ISSN 0265-9247, 12/2016, Volume 38, Issue 12, pp. 1209 - 1217
Post‐translational modifications regulate each step of DNA replication to ensure the faithful transmission of genetic information. In this context, we recently... 
DNA replication | USP7 | SUMO | replisome | ubiquitin | SUMOYLATION DYNAMICS | PCNA | CDT1 PROTEOLYSIS | HUMAN-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | CDK-DEPENDENT PHOSPHORYLATION | DNA-REPLICATION | BIOLOGY | S-PHASE | FORK COLLAPSE | DVC1 C1ORF124 | TARGET PROTEINS | Ubiquitin | Ubiquitination | Animals | Eukaryota - genetics | Humans | Sumoylation | DNA Replication | Small Ubiquitin-Related Modifier Proteins | Eukaryota - metabolism | Antimitotic agents | Dosage and administration | Research | Antineoplastic agents | Factories
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8. Full Text XNaked replication forks break apRPArt
by Fernandez-Capetillo, Oscar and Nussenzweig, André
Cell, ISSN 0092-8674, 11/2013, Volume 155, Issue 5, p. 979
Stalled replication forks occasionally collapse, leading to potentially catastrophic DNA double-strand breaks. Now, Toledo et al. (2013) reveal that fork... 
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9. Full Text Sirt1 improves healthy ageing and protects from metabolic syndrome-associated cancer
by Mulero, Francisca and Herranz, Daniel and Martinez-Pastor, Barbara and Fernandez-Capetillo, Oscar and Cañamero, Marta and Muñoz-Martin, Maribel and Serrano, Manuel
Nature Communications, ISSN 2041-1723, 04/2010, Volume 1, Issue 1, pp. 1 - 8
Genetic overexpression of protein deacetylase Sir2 increases longevity in a variety of lower organisms, and this has prompted interest in the effects of its... 
SURVIVAL | LIFE-SPAN | RESVERATROL | DIET | LIVER-DISEASES | MULTIDISCIPLINARY SCIENCES | MICE | KAPPA-B | TUMORIGENESIS | SMALL-MOLECULE ACTIVATORS | CALORIE RESTRICTION | Diethylnitrosamine - toxicity | Neoplasms - metabolism | Sirtuin 1 - metabolism | Dietary Fats - adverse effects | Glucose Tolerance Test | Neoplasms - etiology | Mice, Inbred C57BL | Male | Metabolic Syndrome - therapy | Mice, Transgenic | Liver Neoplasms - therapy | Longevity - genetics | Sirtuin 1 - genetics | Metabolic Syndrome - complications | Liver Neoplasms - etiology | Animals | Aging - genetics | Aging - physiology | DNA Damage - physiology | DNA Damage - genetics | Female | Mice | Longevity - physiology
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10. Full Text A p53-mediated DNA damage response limits reprogramming to ensure iPS cell genomic integrity
by Marión, Rosa M and Strati, Katerina and Li, Han and Murga, Matilde and Blanco, Raquel and Ortega, Sagrario and Fernandez-Capetillo, Oscar and Serrano, Manuel and Blasco, Maria A
Nature, ISSN 0028-0836, 08/2009, Volume 460, Issue 7259, pp. 1149 - 1153
The reprogramming of differentiated cells to pluripotent cells (induced pluripotent stem (iPS) cells) is known to be an inefficient process. We recently... 
PLURIPOTENT STEM-CELLS | DEFINED FACTORS | MULTIDISCIPLINARY SCIENCES | MOUSE | HUMAN FIBROBLASTS | GENERATION | MICE | ATM | SENESCENCE | TELOMERES | P53 | Pluripotent Stem Cells - cytology | Humans | Cells, Cultured | Tumor Suppressor Protein p53 - metabolism | Genomic Instability - physiology | Male | Tumor Suppressor Protein p53 - deficiency | Tumor Suppressor Protein p53 - genetics | Pluripotent Stem Cells - metabolism | Animals | DNA Damage - physiology | DNA Repair | Chromosome Aberrations | DNA Damage - genetics | Female | Fibroblasts - cytology | Mice | Telomere - metabolism | Genomic Instability - genetics | Apoptosis | Cellular Reprogramming - physiology | Fibroblasts - metabolism | Telomere - genetics | Efficiency | DNA damage | Genomics | Cells
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11. Full Text Lac operator repeats generate a traceable fragile site in mammalian cells
by Fernandez-Capetillo, Oscar and Jacome, Ariana
EMBO reports, ISSN 1469-221X, 10/2011, Volume 12, Issue 10, pp. 1032 - 1038
One limitation for the study of chromosomal fragile sites is that they must be studied on metaphase spreads, after the breakage. We show here that bacterial... 
micronucleus | anaphase bridge | common fragile site | PICH | lac operon | HUMAN-CHROMOSOMES | LOCALIZATION | ACTIVATION | DNA-DAMAGE RESPONSE | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | CANCER | LESIONS | CELL BIOLOGY | ANAPHASE BRIDGES | REPLICATION | STRESS | DNA Breaks - drug effects | NIH 3T3 Cells | Enzyme Inhibitors - pharmacology | Chromosome Fragile Sites - genetics | Lac Operon - genetics | Proto-Oncogene Proteins c-myc - metabolism | Animals | Aphidicolin - pharmacology | Escherichia coli - genetics | Micronuclei, Chromosome-Defective - chemically induced | Mice | Operator Regions, Genetic | Anaphase | Cell division | Signal transduction | Molecular biology | DNA damage | Cell cycle | Scientific Reports
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