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FASEB Journal, ISSN 0892-6638, 09/2014, Volume 28, Issue 9, pp. 3906 - 3918
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2012, Volume 7, Issue 11, p. e49692
Theoretical models suggest that gene silencing at the nuclear periphery may involve "closing" of chromatin by transcriptional repressors, such as histone... 
ORGANIZATION | LEM-DOMAIN PROTEINS | COEXPRESSED GENES | CHROMATIN | DROSOPHILA-MELANOGASTER | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | COMPARTMENTALIZATION | B-TYPE LAMIN | EXPRESSION | GENOME | Lamin Type B - antagonists & inhibitors | Multigene Family | Lamin Type B - genetics | Drosophila Proteins - metabolism | Drosophila melanogaster - genetics | Chromatin Immunoprecipitation | Nuclear Lamina - genetics | Transcription, Genetic | Acetylation | Histone Deacetylase 1 - genetics | Cell Line | Histone Deacetylases - genetics | Drosophila melanogaster - cytology | Gene Expression Regulation | Gene Silencing | Histone Deacetylases - metabolism | Blotting, Western | Lamin Type B - metabolism | Animals | Histones - genetics | RNA, Double-Stranded - genetics | Drosophila melanogaster - enzymology | Chromatin - enzymology | Drosophila Proteins - genetics | Histones - metabolism | Nuclear Lamina - enzymology | Chromatin - genetics | Histone Deacetylase 1 - metabolism | Enzymes | Chromatin | Genetic engineering | Analysis | Genes | Drosophila | Transcription factors | Transcription | Growth rate | Gene regulation | Genomics | Biochemistry | Genomes | Compaction | Proteins | Repressors | Genetics | Medical research | Double-stranded RNA | Gene expression | Gene silencing | Detachment | Insects | Lymphocytes B | Deacetylation | Stem cells | Molecular biology
Journal Article
Journal Article
Nucleic acids symposium series (2004), 2009, Issue 53, pp. 293 - 294
We report that anticancer 5-fluoro-2'-deoxyuridine (FUdR) shows cytotoxicity against mouse cancer cell line FM3A cells, using a progeny clone F28-7 and its... 
Lamin Type B - antagonists & inhibitors | Animals | Lamin Type B - genetics | Lamin Type B - physiology | RNA Interference | Antimetabolites, Antineoplastic - toxicity | Cell Line, Tumor | Mice | Floxuridine - toxicity | Apoptosis | Necrosis
Journal Article
Nucleic acids symposium series (2004), 2008, Issue 52, pp. 627 - 628
We report that anticancer 5-fluoro-2'-deoxyuridine (FUdR) shows cytotoxicity against mouse cancer cell line FM3A cells, using a progeny clone F28-7 and its... 
Lamin Type B - antagonists & inhibitors | Animals | Lamin Type B - genetics | RNA Interference | Antimetabolites, Antineoplastic - toxicity | Cell Line, Tumor | Necrosis - metabolism | Mice | Necrosis - genetics | Apoptosis - physiology | Floxuridine - toxicity | Lamin Type B - metabolism
Journal Article
Journal of the National Cancer Institute, ISSN 0027-8874, 01/2016, Volume 108, Issue 1, p. 1
Journal Article
Circulation, ISSN 0009-7322, 07/2014, Volume 130, Issue 1, pp. 27 - 34
Background-Hutchinson-Gilford progeria syndrome is an ultrarare segmental premature aging disease resulting in early death from heart attack or stroke. There... 
Prenylation | Lonafarnib | Progeria | Atherosclerosis | Aging | Lamins | Kaplan-Meier estimate | atherosclerosis | SYNDROME MUTATION | LONG-TERM | FARNESYLTRANSFERASE INHIBITOR | CARDIAC & CARDIOVASCULAR SYSTEMS | lamins | PROTEIN | lonafarnib | PHENOTYPE | progeria | ZOLEDRONIC ACID | MOUSE MODEL | DISEASE | prenylation | PERIPHERAL VASCULAR DISEASE | aging | OF-THE-LITERATURE | MUTANT LAMIN-A | Atherosclerosis - genetics | Humans | Alkyl and Aryl Transferases - antagonists & inhibitors | Child, Preschool | Male | Young Adult | Piperidines - pharmacology | Nuclear Proteins - deficiency | Diphosphonates - therapeutic use | Imidazoles - therapeutic use | Child | Pravastatin - therapeutic use | Multicenter Studies as Topic - statistics & numerical data | Piperidines - administration & dosage | Progeria - mortality | Pyridines - administration & dosage | Lamin Type A | Genotype | Diphosphonates - administration & dosage | Imidazoles - pharmacology | Protein Precursors - metabolism | Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology | Pravastatin - administration & dosage | Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use | Adolescent | Progeria - complications | Cohort Studies | Hydroxymethylglutaryl-CoA Reductase Inhibitors - administration & dosage | Clinical Trials as Topic - statistics & numerical data | Imidazoles - administration & dosage | Cause of Death | Progeria - drug therapy | Atherosclerosis - etiology | Genes, Dominant | Adult | Female | Drug Therapy, Combination | Nuclear Proteins - genetics | Pyridines - therapeutic use | Pravastatin - pharmacology | Protein Prenylation - drug effects | Protein Precursors - genetics | Kaplan-Meier Estimate | Proportional Hazards Models | Nuclear Proteins - metabolism | Treatment Outcome | Protein Precursors - deficiency | Piperidines - therapeutic use | Dimethylallyltranstransferase - antagonists & inhibitors | Pyridines - pharmacology | Atherosclerosis - prevention & control | Diphosphonates - pharmacology | Care and treatment | Usage | Enzyme inhibitors | Patient outcomes | Genetic aspects | Health aspects | Index Medicus | Abridged Index Medicus | farnesylation | lamin | Hutchinson-Gilford progeria syndrome | FTI
Journal Article
Journal Article
Journal Article
Methods, ISSN 1046-2023, 03/2016, Volume 96, pp. 46 - 58
Hutchinson–Gilford Progeria Syndrome (HGPS) is an early onset lethal premature aging disorder caused by constitutive production of progerin, a mutant form of... 
High-throughput screening | HGPS | High-content imaging | Retinoids | Progerin | FDA-approved compounds | DNA-DAMAGE RESPONSES | DEFECTIVE MATURATION | RESVERATROL | FARNESYLTRANSFERASE INHIBITOR | INSTABILITY | BIOCHEMISTRY & MOLECULAR BIOLOGY | BIOCHEMICAL RESEARCH METHODS | DISEASE PHENOTYPES | SIRT1 | LAMIN B1 | MICE | EXPRESSION | Small Molecule Libraries - pharmacology | Lamin Type B - genetics | Epigenesis, Genetic | Humans | Cellular Senescence - drug effects | Intracellular Signaling Peptides and Proteins - metabolism | Progeria - metabolism | Lamin Type A - antagonists & inhibitors | Cell Nucleus - metabolism | Transfection | Progeria - pathology | Intracellular Signaling Peptides and Proteins - genetics | Fibroblasts - metabolism | Cellular Senescence - genetics | Chromosomal Proteins, Non-Histone - metabolism | Molecular Imaging - methods | Lamin Type A - metabolism | Progeria - genetics | Cell Nucleus - ultrastructure | Fibroblasts - pathology | Plasmids - metabolism | Lamin Type B - metabolism | Chromosomal Proteins, Non-Histone - genetics | High-Throughput Screening Assays | Histones - genetics | Fibroblasts - drug effects | Lamin Type A - genetics | Plasmids - chemistry | Histones - metabolism | Primary Cell Culture | Tumor Suppressor p53-Binding Protein 1 | Cell Nucleus - drug effects | Cell Line, Transformed | Retinoids - pharmacology | Epigenetic inheritance | Medical research | Medicine, Experimental | Skin | Drug discovery | Drug approval
Journal Article
Cell Death and Disease, ISSN 2041-4889, 2016, Volume 7, Issue 2, pp. e2105 - e2105
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2016, Volume 11, Issue 4, p. e0153130
Journal Article