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Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 1/2010, Volume 107, Issue 4, pp. 1506 - 1511
Ataxia-telangiectasia mutated (ATM) is a high molecular weight protein serine/threonine kinase that plays a central role in the maintenance of genomic... 
MicroRNA | Neurons | DNA | DNA damage | Cell lines | Cell cycle | HeLa cells | Ataxia telangiectasia | Neuroblastoma | Three prime untranslated regions | S-phase checkpoint | Radiosensitivity | DNA repair | TARGET | PHOSPHORYLATION | DNA-DAMAGE RESPONSE | MULTIDISCIPLINARY SCIENCES | radiosensitivity | neuroblastoma | ATAXIA-TELANGIECTASIA GENE | ONCOGENE-INDUCED SENESCENCE | IDENTIFICATION | CANCER | IONIZING-RADIATION | TUMORIGENESIS | CHECKPOINTS | Tumor Suppressor Proteins - metabolism | Signal Transduction | Down-Regulation | Humans | Neuroblastoma - genetics | Cell Cycle Proteins - metabolism | Gene Expression Regulation, Neoplastic | Protein-Serine-Threonine Kinases - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Proto-Oncogene Proteins c-myc - metabolism | DNA-Binding Proteins - metabolism | S Phase - radiation effects | Base Sequence | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Cell Line, Tumor | Transcription, Genetic | MicroRNAs - genetics | Neuroblastoma - metabolism | Proto-Oncogene Proteins c-myc - genetics | 3' Untranslated Regions | Protein-Serine-Threonine Kinases - metabolism | Gene mutations | Development and progression | Genetic aspects | Research | Genetic regulation | Properties | Identification and classification | Genotype & phenotype | Genomics | Mutation | Ribonucleic acid--RNA | Kinases | Gene expression | Biological Sciences
Journal Article
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 4/2007, Volume 104, Issue 14, pp. 6007 - 6012
We used antisense morpholino oligonucleotides (AMOs) to redirect and restore normal splicing of three prototypic splicing mutations in the... 
Messenger RNA | Splicing | Reverse transcriptase polymerase chain reaction | Exons | Introns | Cell nucleus | Cell lines | Oligonucleotides | Ataxia telangiectasia | Genetic mutation | Ataxia-telangiectasia mutated | Mutation-based treatment | NERVOUS-SYSTEM | RESTORES DYSTROPHIN EXPRESSION | MULTIDISCIPLINARY SCIENCES | ERYTHROID-CELLS | DEPENDENT APOPTOSIS | OLIGOMERS | PRE-MESSENGER-RNA | BREAST-CANCER | mutation-based treatment | DISEASE | GENE-EXPRESSION | ataxia-telangiectasia mutated | ATAXIA-TELANGIECTASIA | Cell Line | Gamma Rays | Cell Death - radiation effects | Oligonucleotides, Antisense - pharmacology | Protein Kinases - analysis | Humans | Oligonucleotides, Antisense - chemistry | RNA, Messenger - analysis | Reverse Transcriptase Polymerase Chain Reaction | Dose-Response Relationship, Drug | Flow Cytometry | Oligonucleotides, Antisense - genetics | Fluorescein-5-isothiocyanate | RNA Splicing - genetics | Enzyme Induction - drug effects | Ataxia Telangiectasia - genetics | Models, Genetic | Kinetics | Mutation | Protein Kinases - biosynthesis | Fluorescent Antibody Technique, Indirect | Fluorescent Dyes | Care and treatment | Genetic aspects | Research | Gene mutations | RNA splicing | Proteins | Molecules | Pathology | Radiation | Biochemistry | Ribonucleic acid--RNA | Medical disorders | Immune system | Biological Sciences
Journal Article
Cancer Medicine, ISSN 2045-7634, 08/2016, Volume 5, Issue 8, pp. 1962 - 1972
Dysregulated epithelial to mesenchymal transition ( EMT ) in cancer cells endows invasive and metastatic properties upon cancer cells that favor successful... 
Breast | epithelial to mesenchymal transition | non‐small‐cell lung cancer | genomics, transcription factor | non-small-cell lung cancer | RNA, Small Interfering - genetics | Humans | Lung Neoplasms - metabolism | Gene Expression Regulation, Neoplastic | Interferon Regulatory Factors - metabolism | Transcriptome | Co-Repressor Proteins - metabolism | Lung Neoplasms - pathology | Gene Expression Profiling | Epithelial-Mesenchymal Transition - genetics | LIM Domain Proteins - metabolism | Gene Knockdown Techniques | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Reproducibility of Results | Signal Transduction | Carcinoma, Non-Small-Cell Lung - genetics | RNA, Messenger - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | Interferon Regulatory Factors - genetics | Transcription Factors - genetics | Co-Repressor Proteins - genetics | Cell Line, Tumor | LIM Domain Proteins - genetics | Transforming Growth Factor beta - metabolism | Flow cytometry | Cell culture | Phenotypes | Transcription factors | Immunoglobulins | Carcinoma | Mesenchyme | Invasiveness | Transforming growth factor-b | Cytology | Transforming growth factor-a | Metastasis | Drug resistance | Oncostatin M | Gene expression | Metastases | Cell adhesion & migration | DNA microarrays | Cell lines | Stem cells | Hypoxia | Colonization | Cancer
Journal Article
Human Mutation, ISSN 1059-7794, 01/2012, Volume 33, Issue 1, pp. 198 - 208
A recent challenge for investigators studying the progressive neurological disease ataxia-telangiectasia (A-T) is to identify mutations whose effects might be... 
ATM | Large genomic deletions | Ataxia-telangiectasia | Functional analysis of DNA variants | Mutationtargeted therapy | Japanese ATM mutation | POPULATION | ACTIVATION | DNA-DAMAGE | HAPLOTYPES | large genomic deletions | 55-PERCENT | ataxia-telangiectasia | functional analysis of DNA variants | GENE | EXONIC SPLICING ENHANCERS | FAMILIES | VIVO-MORPHOLINOS | GENETICS & HEREDITY | mutation-targeted therapy | AUTOPHOSPHORYLATION | Sequence Deletion | Frameshift Mutation | Oligodeoxyribonucleotides, Antisense - pharmacology | Exons | Humans | Morpholinos - therapeutic use | Molecular Sequence Data | Molecular Targeted Therapy | RNA Splicing | DNA-Binding Proteins - agonists | T-Lymphocytes - metabolism | DNA Mutational Analysis | Gentamicins - pharmacology | T-Lymphocytes - drug effects | Base Sequence | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Ataxia Telangiectasia - drug therapy | T-Lymphocytes - pathology | Cell Line | Gentamicins - therapeutic use | Protein-Serine-Threonine Kinases - genetics | Oligodeoxyribonucleotides, Antisense - therapeutic use | Ataxia Telangiectasia Mutated Proteins | Cell Cycle Proteins - agonists | Codon, Nonsense | DNA-Binding Proteins - genetics | Asian Continental Ancestry Group | Pedigree | Morpholinos - pharmacology | Ataxia Telangiectasia - genetics | Heterozygote | Aminoglycosides - pharmacology | Tumor Suppressor Proteins - agonists | Aminoglycosides - therapeutic use
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