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Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 2280 - 14
Defects in DNA repair can cause various genetic diseases with severe pathological phenotypes. Fanconi anemia ( FA) is a rare disease characterized by bone... 
UBIQUITINATION | DAMAGE RESPONSE | CHROMATIN | CROSS-LINK REPAIR | HUMAN-CELLS | MULTIDISCIPLINARY SCIENCES | SENSITIVITY | HOMOLOGOUS RECOMBINATION | BRCA1 | ENRICHMENT ANALYSIS | ASSOCIATION | Genetic Therapy | Ubiquitin-Specific Proteases - genetics | Fanconi Anemia Complementation Group D2 Protein - genetics | Fanconi Anemia - metabolism | Humans | DNA Repair - physiology | DNA Repair - genetics | Fanconi Anemia Complementation Group C Protein - genetics | Fanconi Anemia Complementation Group A Protein - genetics | Fanconi Anemia Complementation Group D2 Protein - deficiency | Fanconi Anemia Complementation Group A Protein - metabolism | Fanconi Anemia Complementation Group Proteins - metabolism | Ubiquitination | Fanconi Anemia Complementation Group G Protein - genetics | Ubiquitin-Specific Proteases - deficiency | Fanconi Anemia Complementation Group G Protein - deficiency | BRCA1 Protein - metabolism | Fanconi Anemia - genetics | Ubiquitin-Specific Proteases - metabolism | Chromosomal Instability | Rad51 Recombinase - metabolism | Cell Line | Fanconi Anemia Complementation Group Proteins - deficiency | Fanconi Anemia Complementation Group Proteins - genetics | Fanconi Anemia Complementation Group G Protein - metabolism | Gene Knockout Techniques | Fanconi Anemia Complementation Group C Protein - metabolism | Fanconi Anemia Complementation Group D2 Protein - metabolism | Fanconi Anemia Complementation Group A Protein - deficiency | CRISPR-Cas Systems | Fanconi Anemia Complementation Group C Protein - deficiency | Fanconi Anemia - therapy | DNA Damage | Histones - metabolism | Mutation
Journal Article
Molecular Cell, ISSN 1097-2765, 01/2017, Volume 65, Issue 2, pp. 247 - 259
Monoubiquitination and deubiquitination of FANCD2:FANCI heterodimer is central to DNA repair in a pathway that is defective in the cancer predisposition... 
core complex | RING E3 | Fanconi anemia | FANCD2 | deubiquitination | FANCB | enzyme mechanism | monoubiquitination | DNA repair | NUCLEAR ACCUMULATION | MONOUBIQUITINATED FANCD2 | TARGETED DISRUPTION | COMPLEX | DNA-REPAIR PATHWAY | CROSS-LINK REPAIR | BIOCHEMISTRY & MOLECULAR BIOLOGY | PROTEINS | DAMAGE | COMPLEMENTATION GROUP-B | LIGASE | CELL BIOLOGY | Fanconi Anemia Complementation Group D2 Protein - genetics | Fanconi Anemia - metabolism | Humans | Multiprotein Complexes | Protein Multimerization | Substrate Specificity | Fanconi Anemia Complementation Group A Protein - metabolism | DNA-Binding Proteins - metabolism | Fanconi Anemia Complementation Group Proteins - metabolism | Ubiquitination | Transfection | Time Factors | Fanconi Anemia - genetics | Ubiquitin-Specific Proteases - metabolism | Recombinant Proteins - metabolism | Cell Line | Fanconi Anemia Complementation Group Proteins - genetics | Nuclear Proteins - metabolism | Fanconi Anemia Complementation Group G Protein - metabolism | DNA - metabolism | Inhibitor of Differentiation Protein 2 - metabolism | DNA - genetics | Fanconi Anemia Complementation Group C Protein - metabolism | Fanconi Anemia Complementation Group D2 Protein - metabolism | Protein Binding | Fanconi Anemia Complementation Group L Protein - metabolism | Fanconi Anemia Complementation Group E Protein - metabolism | Ubiquitin | Chemotherapy | Ligases | Genomics | Research institutes | Cancer | Fanconi's anemia | Proteins | Medical research | Molecular genetics | Medicine, Experimental
Journal Article
Journal Article
Molecular Cell, ISSN 1097-2765, 10/2016, Volume 64, Issue 2, pp. 388 - 404
Journal Article
Science, ISSN 0036-8075, 7/2010, Volume 329, Issue 5988, pp. 219 - 223
Journal Article
Molecular Cell, ISSN 1097-2765, 01/2015, Volume 57, Issue 1, pp. 150 - 164
We show that central components of the Fanconi anemia (FA) DNA repair pathway, the tumor suppressor proteins FANCI and FANCD2 (the ID complex), are SUMOylated... 
E3 LIGASE | REPAIR | SEGREGASE | PROTEIN | FANCD2 | PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | DVC1 C1ORF124 | RNF4 | IDENTIFICATION | SUMOYLATION | CELL BIOLOGY | Hydroxyurea - pharmacology | Ataxia Telangiectasia Mutated Proteins - metabolism | Fanconi Anemia Complementation Group D2 Protein - genetics | Humans | Ubiquitin - metabolism | Protein Inhibitors of Activated STAT - metabolism | Recombinant Fusion Proteins - metabolism | Small Ubiquitin-Related Modifier Proteins - genetics | Poly-ADP-Ribose Binding Proteins | Fanconi Anemia Complementation Group Proteins - metabolism | Ubiquitination | Cysteine Endopeptidases - metabolism | HEK293 Cells | Protein Inhibitors of Activated STAT - genetics | Protein Interaction Domains and Motifs | Nuclear Proteins - genetics | Signal Transduction | Small Ubiquitin-Related Modifier Proteins - metabolism | Fanconi Anemia Complementation Group Proteins - genetics | Gene Expression Regulation | Nuclear Proteins - metabolism | Ubiquitin - genetics | Transcription Factors - genetics | Transcription Factors - metabolism | Fanconi Anemia Complementation Group D2 Protein - metabolism | Cysteine Endopeptidases - genetics | Cell Line, Tumor | Protein Binding | Recombinant Fusion Proteins - genetics | Sumoylation | DNA Damage | Ataxia Telangiectasia Mutated Proteins - genetics | Ubiquitin | Sumo | Proteases | Ligases | DNA damage | DNA | Molecular biology | Fanconi's anemia
Journal Article
Nature, ISSN 0028-0836, 07/2011, Volume 475, Issue 7354, pp. 53 - 59
Reactive aldehydes are common carcinogens. They are also by-products of several metabolic pathways and, without enzymatic catabolism, may accumulate and cause... 
DNA-ADDUCTS | METABOLISM | MULTIDISCIPLINARY SCIENCES | BONE-MARROW | FETAL ALCOHOL SYNDROME | ETHANOL | CHILDHOOD LEUKEMIA | KNOCKOUT MICE | ACETALDEHYDE | FANCONI-ANEMIA | CONSUMPTION | Embryo, Mammalian - drug effects | Acetaldehyde - metabolism | Clone Cells - drug effects | Teratogens - toxicity | Ethanol - toxicity | Fanconi Anemia Complementation Group D2 Protein - genetics | Weaning | Aldehyde Dehydrogenase, Mitochondrial | Male | DNA Repair - genetics | Aldehydes - metabolism | Aldehydes - antagonists & inhibitors | Fanconi Anemia Complementation Group D2 Protein - deficiency | Precursor Cell Lymphoblastic Leukemia-Lymphoma - chemically induced | Hematopoiesis - drug effects | Fetal Alcohol Spectrum Disorders - etiology | Gene Deletion | Aldehyde Dehydrogenase - deficiency | Embryo Loss - etiology | DNA Damage - genetics | Fanconi Anemia - pathology | Female | Fanconi Anemia - genetics | Aldehyde Dehydrogenase - metabolism | B-Lymphocytes - metabolism | Bone Marrow - drug effects | Cell Line | Cell Survival - drug effects | Aldehydes - toxicity | Bone Marrow - physiopathology | Ethanol - metabolism | Acetaldehyde - toxicity | Embryo Loss - chemically induced | Mice, Inbred C57BL | Aldehyde Dehydrogenase - genetics | Genes, Essential | Embryo, Mammalian - abnormalities | Pregnancy | B-Lymphocytes - drug effects | Animals | Embryo, Mammalian - embryology | Fanconi Anemia Complementation Group D2 Protein - metabolism | Bone Marrow - pathology | Chickens | Alleles | Mice | Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology | Teratogens - metabolism | Causes of | Research | Aldehydes | Health aspects | Fanconi's anemia | Mutation | DNA repair | Stem cells | Cancer
Journal Article
Nature, ISSN 0028-0836, 02/2015, Volume 518, Issue 7538, pp. 258 - 262
Journal Article