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Ataxia-telangiectasia: from a rare disorder to a paradigm for cell signalling and cancer
Nature Reviews Molecular Cell Biology, ISSN 1471-0072, 10/2008, Volume 9, Issue 10, pp. 759 - 769
First described over 80 years ago, ataxia-telangiectasia (A-T) was defined as a clinical entity 50 years ago. Although not encountered by most clinicians, it...
MRE11-RAD50-NBS1 COMPLEX | NIJMEGEN BREAKAGE SYNDROME | DNA-DAMAGE RESPONSE | V(D)J RECOMBINATION | DOUBLE-STRAND BREAKS | ACTIVATES ATM | ATM-DEPENDENT PHOSPHORYLATION | MRN COMPLEX | IONIZING-RADIATION | S-PHASE CHECKPOINT | CELL BIOLOGY | Metabolic Syndrome - etiology | Neoplasms - etiology | Humans | Neoplasms - genetics | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Ataxia Telangiectasia - complications | Ataxia Telangiectasia - physiopathology | DNA-Binding Proteins - physiology | Genetic Predisposition to Disease | Signal Transduction | Protein-Serine-Threonine Kinases - physiology | Insulin Resistance | Protein-Serine-Threonine Kinases - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Tumor Suppressor Proteins - physiology | Animals | Models, Biological | DNA Repair | Ataxia Telangiectasia - genetics | Mice | Protein Processing, Post-Translational | DNA Damage | Mutation | Nerve Degeneration | Cell Cycle Proteins - physiology | Ataxia telangiectasia | Genetic aspects | Cellular signal transduction | Research | DNA damage | Risk factors
MRE11-RAD50-NBS1 COMPLEX | NIJMEGEN BREAKAGE SYNDROME | DNA-DAMAGE RESPONSE | V(D)J RECOMBINATION | DOUBLE-STRAND BREAKS | ACTIVATES ATM | ATM-DEPENDENT PHOSPHORYLATION | MRN COMPLEX | IONIZING-RADIATION | S-PHASE CHECKPOINT | CELL BIOLOGY | Metabolic Syndrome - etiology | Neoplasms - etiology | Humans | Neoplasms - genetics | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Ataxia Telangiectasia - complications | Ataxia Telangiectasia - physiopathology | DNA-Binding Proteins - physiology | Genetic Predisposition to Disease | Signal Transduction | Protein-Serine-Threonine Kinases - physiology | Insulin Resistance | Protein-Serine-Threonine Kinases - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Tumor Suppressor Proteins - physiology | Animals | Models, Biological | DNA Repair | Ataxia Telangiectasia - genetics | Mice | Protein Processing, Post-Translational | DNA Damage | Mutation | Nerve Degeneration | Cell Cycle Proteins - physiology | Ataxia telangiectasia | Genetic aspects | Cellular signal transduction | Research | DNA damage | Risk factors
Journal Article
American Journal of Botany, ISSN 0002-9122, 11/2004, Volume 91, Issue 11, pp. 1846 - 1862
Phylogenetic analysis of 330 plastid matK gene sequences, representing 235 genera from 37 of 39 tribes, and four outgroup taxa from eurosids I supports many...
Legumes | Taxa | Alkaloids | Monophyly | Systematics | Botanical gardens | Parsimony | Phylogenetics | Phylogeny | Plastids | Genera | matK | phylogeny | papilionoid legumes | caesalpinioid legumes | Leguminosae | mimosoid legumes | Mimosoid legumes | Caesalpinioid legumes | Papilionoid legumes | Genetic research | Beans | Mimosaceae | Phylogeny (Botany)
Legumes | Taxa | Alkaloids | Monophyly | Systematics | Botanical gardens | Parsimony | Phylogenetics | Phylogeny | Plastids | Genera | matK | phylogeny | papilionoid legumes | caesalpinioid legumes | Leguminosae | mimosoid legumes | Mimosoid legumes | Caesalpinioid legumes | Papilionoid legumes | Genetic research | Beans | Mimosaceae | Phylogeny (Botany)
Journal Article
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 12/2019, Volume 23, Issue 12, pp. 8151 - 8160
Suppressor of morphogenesis in genitalia 1 (SMG1) and ataxia telangiectasia mutated (ATM) are members of the PI3‐kinase like–kinase (PIKK) family of proteins....
cancer | inflammation | DNA damage | oxidative stress | lymphoma | Flow cytometry | Oxidative stress | Animal models | Lung cancer | Kinases | Experiments | Morphogenesis | Cell cycle | Ataxia | Research centers | Deoxyribonucleic acid--DNA | Genotypes | Medical research | Genitalia | Cytokines | Health risks | Histology | Breast cancer | Inflammation | Embryos | Heterozygosity | Animals | Alleles | Ataxia telangiectasia | Ataxia telangiectasia mutated protein | Software | Lymphomas | Cancer | Tumors | Original
cancer | inflammation | DNA damage | oxidative stress | lymphoma | Flow cytometry | Oxidative stress | Animal models | Lung cancer | Kinases | Experiments | Morphogenesis | Cell cycle | Ataxia | Research centers | Deoxyribonucleic acid--DNA | Genotypes | Medical research | Genitalia | Cytokines | Health risks | Histology | Breast cancer | Inflammation | Embryos | Heterozygosity | Animals | Alleles | Ataxia telangiectasia | Ataxia telangiectasia mutated protein | Software | Lymphomas | Cancer | Tumors | Original
Journal Article
Molecular Therapy, ISSN 1525-0016, 09/2013, Volume 21, Issue 9, pp. 1650 - 1652
Reading of the genetic code through nonsense mutations to restore protein function is a concept that dates back 50 years, with the discovery that streptomycin...
MEDICINE, RESEARCH & EXPERIMENTAL | CODONS | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | GENETICS & HEREDITY | STRESS | ATAXIA-TELANGIECTASIA | CANCER | Triazoles - pharmacology | Acetanilides - pharmacology | Codon, Terminator - drug effects | Humans | Ataxia Telangiectasia - drug therapy | Codon, Nonsense | Thiourea - pharmacology | Ataxia Telangiectasia Mutated Proteins - genetics | Benzodioxoles - pharmacology | Thiourea - analogs & derivatives
MEDICINE, RESEARCH & EXPERIMENTAL | CODONS | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | GENETICS & HEREDITY | STRESS | ATAXIA-TELANGIECTASIA | CANCER | Triazoles - pharmacology | Acetanilides - pharmacology | Codon, Terminator - drug effects | Humans | Ataxia Telangiectasia - drug therapy | Codon, Nonsense | Thiourea - pharmacology | Ataxia Telangiectasia Mutated Proteins - genetics | Benzodioxoles - pharmacology | Thiourea - analogs & derivatives
Journal Article
Cell Cycle, ISSN 1538-4101, 04/2007, Volume 6, Issue 8, pp. 931 - 942
Well before the gene (ATM) mutated in the human genetic disorder ataxia-telangiectasia (A-T) was described it was evident from the clinical, molecular and...
Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | Cell cycle checkpoints | ATM activation | Autophosphorylation | Chromatin | Mre11 complex | DNA damage | TELOMERIC PROTEIN PIN2/TRF1 | DEPENDENT PHOSPHORYLATION | DOUBLE-STRAND BREAKS | HISTONE H2AX | chromatin | S-PHASE CHECKPOINT | CELL BIOLOGY | autophosphorylation | CELL-CYCLE PHASE | IN-VIVO | TELANGIECTASIA-MUTATED ATM | cell cycle checkpoints | IONIZING-RADIATION | ATAXIA-TELANGIECTASIA | Protein Kinases - metabolism | DNA-Binding Proteins - physiology | Phosphorylation | Tumor Suppressor Proteins - metabolism | Humans | Cell Cycle Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins | Protein Processing, Post-Translational - physiology | DNA-Binding Proteins - metabolism | MRE11 Homologue Protein | Animals | DNA Damage - physiology | Models, Biological | Cell Cycle - physiology | Protein-Serine-Threonine Kinases - metabolism
Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | Cell cycle checkpoints | ATM activation | Autophosphorylation | Chromatin | Mre11 complex | DNA damage | TELOMERIC PROTEIN PIN2/TRF1 | DEPENDENT PHOSPHORYLATION | DOUBLE-STRAND BREAKS | HISTONE H2AX | chromatin | S-PHASE CHECKPOINT | CELL BIOLOGY | autophosphorylation | CELL-CYCLE PHASE | IN-VIVO | TELANGIECTASIA-MUTATED ATM | cell cycle checkpoints | IONIZING-RADIATION | ATAXIA-TELANGIECTASIA | Protein Kinases - metabolism | DNA-Binding Proteins - physiology | Phosphorylation | Tumor Suppressor Proteins - metabolism | Humans | Cell Cycle Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins | Protein Processing, Post-Translational - physiology | DNA-Binding Proteins - metabolism | MRE11 Homologue Protein | Animals | DNA Damage - physiology | Models, Biological | Cell Cycle - physiology | Protein-Serine-Threonine Kinases - metabolism
Journal Article
DNA Repair, ISSN 1568-7864, 08/2013, Volume 12, Issue 8, pp. 612 - 619
Patients with ataxia-telangiectasia (A-T) are characterised by genome instability, cancer predisposition and a progressive neurodegeneration. A number of model...
Ataxia-telangiectasia | Atm | Mouse models | Neurodegeneration | PURKINJE-CELLS | ACTIVATION | DNA-DAMAGE | NEURAL-NETWORKS | GENETICS & HEREDITY | ACETYL CYSTEINE | MITOCHONDRIAL DYSFUNCTION | TOXICOLOGY | INCREASED OXIDATIVE STRESS | ATM-DEFICIENT MICE | GENE-PRODUCT | CELLULAR-RESPONSE | Genomic Instability | Neurons - pathology | Brain - cytology | Genetic Predisposition to Disease | Neurodegenerative Diseases - pathology | Ataxia Telangiectasia Mutated Proteins - metabolism | Neurodegenerative Diseases - genetics | Neurons - cytology | Brain - metabolism | Phenotype | Animals | Ataxia Telangiectasia - pathology | Brain - pathology | Ataxia Telangiectasia - genetics | Mice | Neurons - metabolism | Ataxia Telangiectasia Mutated Proteins - genetics | Disease Models, Animal | Ataxia telangiectasia | Ataxia | Nervous system diseases | Automated teller machines | Analysis
Ataxia-telangiectasia | Atm | Mouse models | Neurodegeneration | PURKINJE-CELLS | ACTIVATION | DNA-DAMAGE | NEURAL-NETWORKS | GENETICS & HEREDITY | ACETYL CYSTEINE | MITOCHONDRIAL DYSFUNCTION | TOXICOLOGY | INCREASED OXIDATIVE STRESS | ATM-DEFICIENT MICE | GENE-PRODUCT | CELLULAR-RESPONSE | Genomic Instability | Neurons - pathology | Brain - cytology | Genetic Predisposition to Disease | Neurodegenerative Diseases - pathology | Ataxia Telangiectasia Mutated Proteins - metabolism | Neurodegenerative Diseases - genetics | Neurons - cytology | Brain - metabolism | Phenotype | Animals | Ataxia Telangiectasia - pathology | Brain - pathology | Ataxia Telangiectasia - genetics | Mice | Neurons - metabolism | Ataxia Telangiectasia Mutated Proteins - genetics | Disease Models, Animal | Ataxia telangiectasia | Ataxia | Nervous system diseases | Automated teller machines | Analysis
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 06/2006, Volume 13, Issue 6, pp. 941 - 950
A number of proteins are activated by stress stimuli but none so spectacularly or with the degree of complexity as the tumour suppressor p53 (human p53 gene or...
Cellular stress | Post-translational modifications | Other factors | Cell cycle control | p53 | TRANSCRIPTIONAL ACTIVITY | DAMAGE-INDUCED PHOSPHORYLATION | UBIQUITIN-PROTEIN LIGASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | DNA-DAMAGE | ATM-DEPENDENT PHOSPHORYLATION | cell cycle control | cellular stress | other factors | CELL BIOLOGY | P53-MEDIATED G ARREST | IN-VIVO | TUMOR-SUPPRESSOR | POLY(ADP-RIBOSE) POLYMERASE-1 | post-translational modifications | IONIZING-RADIATION | Protein Kinases - metabolism | Mutagens - toxicity | Phosphorylation | Apoptosis - drug effects | Apoptosis - radiation effects | Cell Cycle - radiation effects | Humans | Tumor Suppressor Protein p53 - metabolism | Ubiquitin - metabolism | Protein Processing, Post-Translational - radiation effects | DNA - radiation effects | Poly(ADP-ribose) Polymerases - metabolism | Animals | Protein Processing, Post-Translational - drug effects | Acetylation | DNA Damage | Cell Cycle - drug effects | Proto-Oncogene Proteins c-mdm2 - metabolism | DNA - drug effects
Cellular stress | Post-translational modifications | Other factors | Cell cycle control | p53 | TRANSCRIPTIONAL ACTIVITY | DAMAGE-INDUCED PHOSPHORYLATION | UBIQUITIN-PROTEIN LIGASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | DNA-DAMAGE | ATM-DEPENDENT PHOSPHORYLATION | cell cycle control | cellular stress | other factors | CELL BIOLOGY | P53-MEDIATED G ARREST | IN-VIVO | TUMOR-SUPPRESSOR | POLY(ADP-RIBOSE) POLYMERASE-1 | post-translational modifications | IONIZING-RADIATION | Protein Kinases - metabolism | Mutagens - toxicity | Phosphorylation | Apoptosis - drug effects | Apoptosis - radiation effects | Cell Cycle - radiation effects | Humans | Tumor Suppressor Protein p53 - metabolism | Ubiquitin - metabolism | Protein Processing, Post-Translational - radiation effects | DNA - radiation effects | Poly(ADP-ribose) Polymerases - metabolism | Animals | Protein Processing, Post-Translational - drug effects | Acetylation | DNA Damage | Cell Cycle - drug effects | Proto-Oncogene Proteins c-mdm2 - metabolism | DNA - drug effects
Journal Article
Science, ISSN 0036-8075, 10/2010, Volume 330, Issue 6003, pp. 517 - 521
The ataxia-telangiectasia mutated (ATM) protein kinase is activated by DNA double-strand breaks (DSBs) through the Mre11-Rad50-Nbs1 (MRN) DNA repair complex...
Oxidative stress | Phosphorylation | Lymphocytes | DNA | DNA damage | REPORTS | Disulfides | Ataxia telangiectasia | Oxidation | Dimers | Genetic mutation | CELLS | PROTEIN | ANTIOXIDANTS | PHOSPHORYLATION | MANGANESE | TELANGIECTASIA GENE-PRODUCT | MULTIDISCIPLINARY SCIENCES | DNA-DAMAGE | PURIFICATION | DEFICIENT MICE | ATAXIA-TELANGIECTASIA | Disulfides - metabolism | Tumor Suppressor Proteins - metabolism | Oxidative Stress | Humans | Hydrogen Peroxide | Cell Cycle Proteins - metabolism | DNA Repair Enzymes - genetics | Protein-Serine-Threonine Kinases - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | DNA Breaks, Double-Stranded | DNA-Binding Proteins - metabolism | MRE11 Homologue Protein | Animals | DNA Repair | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Ataxia Telangiectasia - genetics | Cysteine - metabolism | Enzyme Activation | Mutation | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Ataxia Telangiectasia - enzymology | Influence | Genetic aspects | Research | Properties | Protein kinases | Cellular biology | Kinases | Stresses | Cysteine | Pathways | Deoxyribonucleic acid | Cascades | Activation | Automated teller machines
Oxidative stress | Phosphorylation | Lymphocytes | DNA | DNA damage | REPORTS | Disulfides | Ataxia telangiectasia | Oxidation | Dimers | Genetic mutation | CELLS | PROTEIN | ANTIOXIDANTS | PHOSPHORYLATION | MANGANESE | TELANGIECTASIA GENE-PRODUCT | MULTIDISCIPLINARY SCIENCES | DNA-DAMAGE | PURIFICATION | DEFICIENT MICE | ATAXIA-TELANGIECTASIA | Disulfides - metabolism | Tumor Suppressor Proteins - metabolism | Oxidative Stress | Humans | Hydrogen Peroxide | Cell Cycle Proteins - metabolism | DNA Repair Enzymes - genetics | Protein-Serine-Threonine Kinases - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | DNA Breaks, Double-Stranded | DNA-Binding Proteins - metabolism | MRE11 Homologue Protein | Animals | DNA Repair | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Ataxia Telangiectasia - genetics | Cysteine - metabolism | Enzyme Activation | Mutation | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Ataxia Telangiectasia - enzymology | Influence | Genetic aspects | Research | Properties | Protein kinases | Cellular biology | Kinases | Stresses | Cysteine | Pathways | Deoxyribonucleic acid | Cascades | Activation | Automated teller machines
Journal Article
Lancet, The, ISSN 0140-6736, 2016, Volume 388, Issue 10049, pp. 1057 - 1066
Summary Background The absence of trial data comparing robot-assisted laparoscopic prostatectomy and open radical retropubic prostatectomy is a crucial...
Internal Medicine | LYMPH-NODE DISSECTION | TRIAL | MEDICINE, GENERAL & INTERNAL | METAANALYSIS | POSITIVE SURGICAL MARGINS | COMPLICATIONS | QUALITY-OF-LIFE | SCALE | INDEX | CANCER | ERECTILE DYSFUNCTION | Postoperative Complications - etiology | Prostatectomy - methods | Robotic Surgical Procedures | Prostatic Neoplasms - surgery | Comorbidity | Humans | Middle Aged | Self Report | Male | Treatment Outcome | Laparoscopy | Prostatic Neoplasms - physiopathology | Prostatectomy - adverse effects | Penile Erection | Quality of Life | Adult | Aged | Urination | Queensland | Robotic surgery | Clinical trials | Laparoscopic surgery | Prostate cancer | Robots | Analysis | Studies | Surgical outcomes | Surgery | Patients | Prostate | Robotics | Quality of life
Internal Medicine | LYMPH-NODE DISSECTION | TRIAL | MEDICINE, GENERAL & INTERNAL | METAANALYSIS | POSITIVE SURGICAL MARGINS | COMPLICATIONS | QUALITY-OF-LIFE | SCALE | INDEX | CANCER | ERECTILE DYSFUNCTION | Postoperative Complications - etiology | Prostatectomy - methods | Robotic Surgical Procedures | Prostatic Neoplasms - surgery | Comorbidity | Humans | Middle Aged | Self Report | Male | Treatment Outcome | Laparoscopy | Prostatic Neoplasms - physiopathology | Prostatectomy - adverse effects | Penile Erection | Quality of Life | Adult | Aged | Urination | Queensland | Robotic surgery | Clinical trials | Laparoscopic surgery | Prostate cancer | Robots | Analysis | Studies | Surgical outcomes | Surgery | Patients | Prostate | Robotics | Quality of life
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Stem Cell Research and Therapy, ISSN 1757-6512, 11/2018, Volume 9, Issue 1, pp. 311 - 14
Pulmonary fibrosis induced by silica dust is an irreversible, chronic, and fibroproliferative lung disease with no effective treatment at present. Previous...
Animal model | Bone marrow mesenchymal stem/stromal cells (BMSCs) | Transplantation | Cell therapy | Pulmonary fibrosis | Silicosis | Cyclin D1 - metabolism | Lung - pathology | Phosphorylation | Cell Proliferation | Bone Marrow Cells - cytology | Hydroxyproline - metabolism | Male | Tomography, X-Ray Computed | Lung - diagnostic imaging | Pulmonary Fibrosis - pathology | Glycogen Synthase Kinase 3 beta - metabolism | Rats, Sprague-Dawley | beta Catenin - metabolism | Animals | Pulmonary Fibrosis - diagnostic imaging | Silicon Dioxide | Mesenchymal Stem Cells - cytology | Epithelial-Mesenchymal Transition | Pulmonary Fibrosis - chemically induced | Pulmonary Fibrosis - metabolism | Mesenchymal Stem Cell Transplantation | Suspensions | Wnt Signaling Pathway
Animal model | Bone marrow mesenchymal stem/stromal cells (BMSCs) | Transplantation | Cell therapy | Pulmonary fibrosis | Silicosis | Cyclin D1 - metabolism | Lung - pathology | Phosphorylation | Cell Proliferation | Bone Marrow Cells - cytology | Hydroxyproline - metabolism | Male | Tomography, X-Ray Computed | Lung - diagnostic imaging | Pulmonary Fibrosis - pathology | Glycogen Synthase Kinase 3 beta - metabolism | Rats, Sprague-Dawley | beta Catenin - metabolism | Animals | Pulmonary Fibrosis - diagnostic imaging | Silicon Dioxide | Mesenchymal Stem Cells - cytology | Epithelial-Mesenchymal Transition | Pulmonary Fibrosis - chemically induced | Pulmonary Fibrosis - metabolism | Mesenchymal Stem Cell Transplantation | Suspensions | Wnt Signaling Pathway
Journal Article