Science, ISSN 0036-8075, 2/2013, Volume 339, Issue 6120, pp. 711 - 715
DNA double-strand breaks (DSBs) represent a threat to the genome because they can lead to the loss of genetic information and chromosome rearrangements. The...
Proteins | Phosphorylation | B lymphocytes | DNA damage | DNA | REPORTS | Cell cycle | Genomes | DNA repair | Chromosomes | Genotypes | B-LYMPHOCYTES | RECOMBINATION | REGULATOR | REPAIR | REPLICATION | 53BP1 | MULTIDISCIPLINARY SCIENCES | END RESECTION | AID | DAMAGE | TELOMERES | Genomic Instability | Tumor Suppressor Proteins - antagonists & inhibitors | DNA Breaks, Double-Stranded | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | S Phase | Protein-Serine-Threonine Kinases - antagonists & inhibitors | G2 Phase | Telomere-Binding Proteins - metabolism | Immunoglobulin Class Switching | B-Lymphocytes - metabolism | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Chromosomal Proteins, Non-Histone - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Ataxia Telangiectasia Mutated Proteins | DNA - metabolism | G1 Phase | Animals | B-Lymphocytes - immunology | DNA Repair | Mice | Tumor Suppressor p53-Binding Protein 1 | Immunoglobulins | Research | Properties | Genomics | Breaking | Deoxyribonucleic acid | Damage | Online | Repair | Switching
Proteins | Phosphorylation | B lymphocytes | DNA damage | DNA | REPORTS | Cell cycle | Genomes | DNA repair | Chromosomes | Genotypes | B-LYMPHOCYTES | RECOMBINATION | REGULATOR | REPAIR | REPLICATION | 53BP1 | MULTIDISCIPLINARY SCIENCES | END RESECTION | AID | DAMAGE | TELOMERES | Genomic Instability | Tumor Suppressor Proteins - antagonists & inhibitors | DNA Breaks, Double-Stranded | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | S Phase | Protein-Serine-Threonine Kinases - antagonists & inhibitors | G2 Phase | Telomere-Binding Proteins - metabolism | Immunoglobulin Class Switching | B-Lymphocytes - metabolism | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Chromosomal Proteins, Non-Histone - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Ataxia Telangiectasia Mutated Proteins | DNA - metabolism | G1 Phase | Animals | B-Lymphocytes - immunology | DNA Repair | Mice | Tumor Suppressor p53-Binding Protein 1 | Immunoglobulins | Research | Properties | Genomics | Breaking | Deoxyribonucleic acid | Damage | Online | Repair | Switching
Journal Article
Nature Immunology, ISSN 1529-2908, 01/2011, Volume 12, Issue 1, pp. 62 - 69
The cytidine deaminase AID hypermutates immunoglobulin genes but can also target oncogenes, leading to tumorigenesis. The extent of AID's promiscuity and its...
RNA-POLYMERASE-II | ACTIVATION-INDUCED DEAMINASE | SOMATIC HYPERMUTATION | KINASE-A | REPLICATION PROTEIN-A | IMMUNOGLOBULIN GENES | C-MYC | IG GENES | CLASS-SWITCH RECOMBINATION | IMMUNOLOGY | CELL LYMPHOMAS | Lipopolysaccharides - metabolism | Chromatin Assembly and Disassembly - genetics | Lipopolysaccharides - immunology | Promoter Regions, Genetic - genetics | Cell Transformation, Neoplastic - genetics | Replication Protein A - genetics | B-Lymphocytes - pathology | Immunoglobulin Class Switching | B-Lymphocytes - metabolism | Genes, Immunoglobulin - genetics | Somatic Hypermutation, Immunoglobulin | Cytidine Deaminase - genetics | Interleukin-4 - metabolism | Mice, Inbred C57BL | Cells, Cultured | Replication Protein A - metabolism | Mice, Knockout | Interleukin-4 - immunology | Cell Transformation, Neoplastic - immunology | Animals | B-Lymphocytes - immunology | Cytidine Deaminase - metabolism | Genes, myc - genetics | High-Throughput Nucleotide Sequencing | Mice | Enzymes | Usage | Gene mutations | Physiological aspects | Hydrolases | Genetic aspects | B cells | Research | Nucleotide sequencing | Health aspects
RNA-POLYMERASE-II | ACTIVATION-INDUCED DEAMINASE | SOMATIC HYPERMUTATION | KINASE-A | REPLICATION PROTEIN-A | IMMUNOGLOBULIN GENES | C-MYC | IG GENES | CLASS-SWITCH RECOMBINATION | IMMUNOLOGY | CELL LYMPHOMAS | Lipopolysaccharides - metabolism | Chromatin Assembly and Disassembly - genetics | Lipopolysaccharides - immunology | Promoter Regions, Genetic - genetics | Cell Transformation, Neoplastic - genetics | Replication Protein A - genetics | B-Lymphocytes - pathology | Immunoglobulin Class Switching | B-Lymphocytes - metabolism | Genes, Immunoglobulin - genetics | Somatic Hypermutation, Immunoglobulin | Cytidine Deaminase - genetics | Interleukin-4 - metabolism | Mice, Inbred C57BL | Cells, Cultured | Replication Protein A - metabolism | Mice, Knockout | Interleukin-4 - immunology | Cell Transformation, Neoplastic - immunology | Animals | B-Lymphocytes - immunology | Cytidine Deaminase - metabolism | Genes, myc - genetics | High-Throughput Nucleotide Sequencing | Mice | Enzymes | Usage | Gene mutations | Physiological aspects | Hydrolases | Genetic aspects | B cells | Research | Nucleotide sequencing | Health aspects
Journal Article
3.
Full Text
c-Myc Is a Universal Amplifier of Expressed Genes in Lymphocytes and Embryonic Stem Cells
Cell, ISSN 0092-8674, 09/2012, Volume 151, Issue 1, pp. 68 - 79
The c-Myc HLH-bZIP protein has been implicated in physiological or pathological growth, proliferation, apoptosis, metabolism, and differentiation at the...
ONCOGENES | LYMPHOMA CELLS | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MOUSE | GRAPHICAL USER-INTERFACE | TRANSCRIPTION FACTOR MYC | FIBROBLASTS | GENOME | RNA-POLYMERASE | REVEALS | CELL BIOLOGY | Lymphocytes - metabolism | Embryonic Stem Cells - metabolism | Promoter Regions, Genetic | Animals | Humans | Transcriptional Activation | Mice | Spleen - cytology | DNA-Directed RNA Polymerases - metabolism | Genome | Proto-Oncogene Proteins c-myc - metabolism | B-Lymphocytes - metabolism | Chromatin | RNA | Lymphocytes | Analysis | Genes | Genomics | Genetic research | Physiological aspects | Embryonic stem cells
ONCOGENES | LYMPHOMA CELLS | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MOUSE | GRAPHICAL USER-INTERFACE | TRANSCRIPTION FACTOR MYC | FIBROBLASTS | GENOME | RNA-POLYMERASE | REVEALS | CELL BIOLOGY | Lymphocytes - metabolism | Embryonic Stem Cells - metabolism | Promoter Regions, Genetic | Animals | Humans | Transcriptional Activation | Mice | Spleen - cytology | DNA-Directed RNA Polymerases - metabolism | Genome | Proto-Oncogene Proteins c-myc - metabolism | B-Lymphocytes - metabolism | Chromatin | RNA | Lymphocytes | Analysis | Genes | Genomics | Genetic research | Physiological aspects | Embryonic stem cells
Journal Article
Immunity, ISSN 1074-7613, 2010, Volume 32, Issue 6, pp. 828 - 839
Although the cellular concentration of miRNAs is critical to their function, how miRNA expression and abundance are regulated during ontogeny is unclear. We...
SYSBIO | MOLIMMUNO | POSTTRANSCRIPTIONAL REGULATION | HOST GENES | STEM-CELLS | CAENORHABDITIS-ELEGANS | SMALL RNAS | INDUCED CYTIDINE DEAMINASE | MOUSE OOCYTES | B-CELL DIFFERENTIATION | C-ELEGANS | IMMUNOLOGY | T-CELLS | Gene Expression | Animals | Gene Expression Regulation - genetics | Lymphocytes | Epigenesis, Genetic | Humans | Lymphopoiesis - genetics | Mice | MicroRNAs - genetics | Reverse Transcriptase Polymerase Chain Reaction | Genetic disorders | Messenger RNA | Oncology, Experimental | Genetic research | Biosynthesis | Research | Gene expression | Cancer | Proteins | Spleen | MicroRNAs | Stem cells | Bone marrow | Genomes | RNA polymerase | Immune system
SYSBIO | MOLIMMUNO | POSTTRANSCRIPTIONAL REGULATION | HOST GENES | STEM-CELLS | CAENORHABDITIS-ELEGANS | SMALL RNAS | INDUCED CYTIDINE DEAMINASE | MOUSE OOCYTES | B-CELL DIFFERENTIATION | C-ELEGANS | IMMUNOLOGY | T-CELLS | Gene Expression | Animals | Gene Expression Regulation - genetics | Lymphocytes | Epigenesis, Genetic | Humans | Lymphopoiesis - genetics | Mice | MicroRNAs - genetics | Reverse Transcriptase Polymerase Chain Reaction | Genetic disorders | Messenger RNA | Oncology, Experimental | Genetic research | Biosynthesis | Research | Gene expression | Cancer | Proteins | Spleen | MicroRNAs | Stem cells | Bone marrow | Genomes | RNA polymerase | Immune system
Journal Article
Nature, ISSN 0028-0836, 04/2012, Volume 484, Issue 7392, pp. 69 - 74
Recurrent chromosomal translocations underlie both haematopoietic and solid tumours. Their origin has been ascribed to selection of random rearrangements,...
ORGANIZATION | CELLS | HUMAN GENOME | MULTIDISCIPLINARY SCIENCES | BREAKS | CLASS-SWITCH RECOMBINATION | MECHANISMS | AID | IDENTIFICATION | REARRANGEMENTS | SEQUENCING REVEALS | Chromosome Positioning | B-Lymphocytes - cytology | Chromosomes, Mammalian - genetics | Cytidine Deaminase - genetics | Cells, Cultured | Genome - genetics | Replication Protein A - metabolism | DNA Breaks, Double-Stranded | Animals | Cell Nucleus - metabolism | Cell Nucleus - genetics | Cytidine Deaminase - metabolism | Genes, myc - genetics | Cytidine Deaminase - deficiency | DNA Damage - genetics | Mice | B-Lymphocytes - pathology | Chromosomes, Mammalian - metabolism | B-Lymphocytes - metabolism | Immunoglobulin Heavy Chains - genetics | Translocation, Genetic - genetics | Translocation (Genetics) | DNA damage | Physiological aspects | Development and progression | Genetic aspects | B cells | Health aspects | Cancer | Proteins | Software | Immunology | Chromosomes | Genes
ORGANIZATION | CELLS | HUMAN GENOME | MULTIDISCIPLINARY SCIENCES | BREAKS | CLASS-SWITCH RECOMBINATION | MECHANISMS | AID | IDENTIFICATION | REARRANGEMENTS | SEQUENCING REVEALS | Chromosome Positioning | B-Lymphocytes - cytology | Chromosomes, Mammalian - genetics | Cytidine Deaminase - genetics | Cells, Cultured | Genome - genetics | Replication Protein A - metabolism | DNA Breaks, Double-Stranded | Animals | Cell Nucleus - metabolism | Cell Nucleus - genetics | Cytidine Deaminase - metabolism | Genes, myc - genetics | Cytidine Deaminase - deficiency | DNA Damage - genetics | Mice | B-Lymphocytes - pathology | Chromosomes, Mammalian - metabolism | B-Lymphocytes - metabolism | Immunoglobulin Heavy Chains - genetics | Translocation, Genetic - genetics | Translocation (Genetics) | DNA damage | Physiological aspects | Development and progression | Genetic aspects | B cells | Health aspects | Cancer | Proteins | Software | Immunology | Chromosomes | Genes
Journal Article
Cell Reports, ISSN 2211-1247, 05/2013, Volume 3, Issue 5, pp. 1678 - 1689
The “CTCF code” hypothesis posits that CTCF pleiotropic functions are driven by recognition of diverse sequences through combinatorial use of its 11 zinc...
ZINC FINGERS | PROTEIN-DNA INTERACTIONS | GENE | CHROMATIN | EMBRYONIC STEM-CELLS | TRANSCRIPTION | SITES | BINDING PROTEIN | IDENTIFICATION | REGULATORY ELEMENTS | CELL BIOLOGY | Repressor Proteins - chemistry | Mice, Inbred C57BL | Repressor Proteins - genetics | Male | Chromosome Mapping | Animals | Nucleotide Motifs | CCCTC-Binding Factor | Zinc Fingers - genetics | Mice | Genome | Binding Sites | B-Lymphocytes - metabolism | Repressor Proteins - metabolism | Photobleaching
ZINC FINGERS | PROTEIN-DNA INTERACTIONS | GENE | CHROMATIN | EMBRYONIC STEM-CELLS | TRANSCRIPTION | SITES | BINDING PROTEIN | IDENTIFICATION | REGULATORY ELEMENTS | CELL BIOLOGY | Repressor Proteins - chemistry | Mice, Inbred C57BL | Repressor Proteins - genetics | Male | Chromosome Mapping | Animals | Nucleotide Motifs | CCCTC-Binding Factor | Zinc Fingers - genetics | Mice | Genome | Binding Sites | B-Lymphocytes - metabolism | Repressor Proteins - metabolism | Photobleaching
Journal Article
Cancer Science, ISSN 1347-9032, 08/2017, Volume 108, Issue 8, pp. 1556 - 1564
B‐cell lymphoma 6 (BCL6) attenuates DNA damage response (DDR) through gene repression and facilitates tolerance to genomic instability during immunoglobulin...
multiple myeloma | ATM | BCL6 | DNA repair | IL‐6 | IL-6 | MULTIPLE-MYELOMA | CYTIDINE DEAMINASE AID | ACTIVATION | CLASS SWITCH RECOMBINATION | TRANSLOCATIONS | GENOMIC INSTABILITY | ONCOLOGY | SPI-B | BCL6 BTB DOMAIN | DIFFERENTIATION | Genomic Instability | Up-Regulation | Cytidine Deaminase - genetics | Humans | Gene Expression Regulation, Neoplastic | Gene Expression Profiling - methods | Gene Regulatory Networks | Proto-Oncogene Proteins c-bcl-6 - genetics | Sequence Analysis, RNA - methods | Phenotype | Cell Line, Tumor | DNA Damage | Ataxia Telangiectasia Mutated Proteins - genetics | Multiple Myeloma - genetics | RNA | DNA damage | Genes | Multiple myeloma | Development and progression | B cells | Genetic transcription | Interleukins | Analysis | DNA | Genetic research | Lymphomas | Genetic aspects | Cancer | Flow cytometry | Genomes | Genomic instability | Cell cycle | Bone marrow | Ataxia | Deoxyribonucleic acid--DNA | Medical research | Immunoglobulins | Cell differentiation | Gene expression | Lymphoma | Immunological tolerance | Studies | Gene silencing | Lymphocytes B | External stimuli | Plasma cells | Ataxia telangiectasia mutated protein | Mutation | Cytidine deaminase | Bcl-6 protein | Original
multiple myeloma | ATM | BCL6 | DNA repair | IL‐6 | IL-6 | MULTIPLE-MYELOMA | CYTIDINE DEAMINASE AID | ACTIVATION | CLASS SWITCH RECOMBINATION | TRANSLOCATIONS | GENOMIC INSTABILITY | ONCOLOGY | SPI-B | BCL6 BTB DOMAIN | DIFFERENTIATION | Genomic Instability | Up-Regulation | Cytidine Deaminase - genetics | Humans | Gene Expression Regulation, Neoplastic | Gene Expression Profiling - methods | Gene Regulatory Networks | Proto-Oncogene Proteins c-bcl-6 - genetics | Sequence Analysis, RNA - methods | Phenotype | Cell Line, Tumor | DNA Damage | Ataxia Telangiectasia Mutated Proteins - genetics | Multiple Myeloma - genetics | RNA | DNA damage | Genes | Multiple myeloma | Development and progression | B cells | Genetic transcription | Interleukins | Analysis | DNA | Genetic research | Lymphomas | Genetic aspects | Cancer | Flow cytometry | Genomes | Genomic instability | Cell cycle | Bone marrow | Ataxia | Deoxyribonucleic acid--DNA | Medical research | Immunoglobulins | Cell differentiation | Gene expression | Lymphoma | Immunological tolerance | Studies | Gene silencing | Lymphocytes B | External stimuli | Plasma cells | Ataxia telangiectasia mutated protein | Mutation | Cytidine deaminase | Bcl-6 protein | Original
Journal Article
Cell, ISSN 0092-8674, 04/2010, Volume 141, Issue 3, pp. 419 - 431
The critical initial step in V(D)J recombination, binding of RAG1 and RAG2 to recombination signal sequences flanking antigen receptor V, D, and J gene...
PROTEINS | MOLIMMUNO | DNA | Proteins | Molimmuno | CHROMOSOMAL TRANSLOCATIONS | REPAIR | HISTONE H3 | ACTIVE-SITE | BIOCHEMISTRY & MOLECULAR BIOLOGY | ACCESSIBILITY | V(D)J RECOMBINATION | HEAVY-CHAIN LOCUS | SYNAPTIC COMPLEX | CLEAVAGE | DNA BREAKS | CELL BIOLOGY | Gene Rearrangement, T-Lymphocyte | Homeodomain Proteins - metabolism | Mice, Inbred C57BL | Mice, Transgenic | Genes, T-Cell Receptor beta | DNA-Binding Proteins - metabolism | Genes, Immunoglobulin Heavy Chain | Immunoglobulin kappa-Chains - genetics | Animals | Recombination, Genetic | Genes, T-Cell Receptor alpha | Gene Rearrangement, B-Lymphocyte | Mice | Antigens | Chromatin | Anopheles | Lysine | Oncology, Experimental | Skin diseases | Research | Cancer | Protein binding
PROTEINS | MOLIMMUNO | DNA | Proteins | Molimmuno | CHROMOSOMAL TRANSLOCATIONS | REPAIR | HISTONE H3 | ACTIVE-SITE | BIOCHEMISTRY & MOLECULAR BIOLOGY | ACCESSIBILITY | V(D)J RECOMBINATION | HEAVY-CHAIN LOCUS | SYNAPTIC COMPLEX | CLEAVAGE | DNA BREAKS | CELL BIOLOGY | Gene Rearrangement, T-Lymphocyte | Homeodomain Proteins - metabolism | Mice, Inbred C57BL | Mice, Transgenic | Genes, T-Cell Receptor beta | DNA-Binding Proteins - metabolism | Genes, Immunoglobulin Heavy Chain | Immunoglobulin kappa-Chains - genetics | Animals | Recombination, Genetic | Genes, T-Cell Receptor alpha | Gene Rearrangement, B-Lymphocyte | Mice | Antigens | Chromatin | Anopheles | Lysine | Oncology, Experimental | Skin diseases | Research | Cancer | Protein binding
Journal Article
Cell, ISSN 0092-8674, 2011, Volume 147, Issue 1, pp. 95 - 106
Chromosomal rearrangements, including translocations, require formation and joining of DNA double strand breaks (DSBs). These events disrupt the integrity of...
GENOMIC INSTABILITY | CYTIDINE DEAMINASE AID | SOMATIC HYPERMUTATION | CELL LYMPHOMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | C-MYC | CANCER GENOME | CLASS-SWITCH RECOMBINATION | FOLLICULAR LYMPHOMA | BCL6 GENE | DNA BREAKS | CELL BIOLOGY | Translocation, Genetic | Humans | Cells, Cultured | Spleen - cytology | Genes, myc | Animals | Mutagenesis | Neoplasms - genetics | Cytidine Deaminase - metabolism | Mice | Genome | Sequence Analysis, DNA - methods | B-Lymphocytes - metabolism | Immunoglobulin Heavy Chains - genetics | Sarcoma | Lymphocytes | Oncology, Experimental | Genomics | Leukemia | Stem cells | Lymphomas | Genomes | Research | Cancer | Chromosome translocations | Territory | double prime B-cell lymphoma | Lymphocytes B | Transcription | DNA damage | Activation-induced cytidine deaminase | Chromosome rearrangements
GENOMIC INSTABILITY | CYTIDINE DEAMINASE AID | SOMATIC HYPERMUTATION | CELL LYMPHOMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | C-MYC | CANCER GENOME | CLASS-SWITCH RECOMBINATION | FOLLICULAR LYMPHOMA | BCL6 GENE | DNA BREAKS | CELL BIOLOGY | Translocation, Genetic | Humans | Cells, Cultured | Spleen - cytology | Genes, myc | Animals | Mutagenesis | Neoplasms - genetics | Cytidine Deaminase - metabolism | Mice | Genome | Sequence Analysis, DNA - methods | B-Lymphocytes - metabolism | Immunoglobulin Heavy Chains - genetics | Sarcoma | Lymphocytes | Oncology, Experimental | Genomics | Leukemia | Stem cells | Lymphomas | Genomes | Research | Cancer | Chromosome translocations | Territory | double prime B-cell lymphoma | Lymphocytes B | Transcription | DNA damage | Activation-induced cytidine deaminase | Chromosome rearrangements
Journal Article
Cell, ISSN 0092-8674, 10/2010, Volume 143, Issue 1, pp. 122 - 133
Activation-induced cytidine deaminase (AID) initiates antibody gene diversification by creating U:G mismatches. However, AID is not specific for antibody...
MOLIMMUNO | DNA | Molimmuno | TRANSCRIPTION ELONGATION-FACTOR | PROTEIN-KINASE-A | CENTER B-CELLS | SOMATIC HYPERMUTATION | IMMUNOGLOBULIN GENES | BIOCHEMISTRY & MOLECULAR BIOLOGY | C-MYC | ANTIBODY DIVERSIFICATION ENZYME | CLASS-SWITCH RECOMBINATION | SINGLE-STRANDED-DNA | P-TEFB | CELL BIOLOGY | Cell Line | Chromosomal Proteins, Non-Histone - metabolism | Humans | Immunoglobulins - genetics | RNA Polymerase II - metabolism | Transcriptional Elongation Factors - metabolism | Animals | Cytidine Deaminase - metabolism | Cell Line, Tumor | Mice | Immunoglobulin Class Switching | B-Lymphocytes - metabolism | Fibroblasts - metabolism | Viral antibodies | RNA | Oncology, Experimental | Antibodies | Skin diseases | Research | Cancer
MOLIMMUNO | DNA | Molimmuno | TRANSCRIPTION ELONGATION-FACTOR | PROTEIN-KINASE-A | CENTER B-CELLS | SOMATIC HYPERMUTATION | IMMUNOGLOBULIN GENES | BIOCHEMISTRY & MOLECULAR BIOLOGY | C-MYC | ANTIBODY DIVERSIFICATION ENZYME | CLASS-SWITCH RECOMBINATION | SINGLE-STRANDED-DNA | P-TEFB | CELL BIOLOGY | Cell Line | Chromosomal Proteins, Non-Histone - metabolism | Humans | Immunoglobulins - genetics | RNA Polymerase II - metabolism | Transcriptional Elongation Factors - metabolism | Animals | Cytidine Deaminase - metabolism | Cell Line, Tumor | Mice | Immunoglobulin Class Switching | B-Lymphocytes - metabolism | Fibroblasts - metabolism | Viral antibodies | RNA | Oncology, Experimental | Antibodies | Skin diseases | Research | Cancer
Journal Article