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1. Full Text mTOR Inhibition Prevents Epithelial Stem Cell Senescence and Protects from Radiation-Induced Mucositis
by Iglesias-Bartolome, Ramiro and Patel, Vyomesh and Cotrim, Ana and Leelahavanichkul, Kantima and Molinolo, Alfredo A and Mitchell, James B and Gutkind, J. Silvio
Cell Stem Cell, ISSN 1934-5909, 09/2012, Volume 11, Issue 3, pp. 401 - 414
The integrity of the epidermis and mucosal epithelia is highly dependent on resident self-renewing stem cells, which makes them vulnerable to physical and... 
MAMMALIAN TARGET | CANCER PATIENTS | RAPAMYCIN | HEAD | AGING PHENOTYPES | MANGANESE SUPEROXIDE-DISMUTASE | STRESS-RESPONSE | TUMOR | NECK | SKIN | CELL & TISSUE ENGINEERING | CELL BIOLOGY | Cell Death - radiation effects | TOR Serine-Threonine Kinases - metabolism | Keratinocytes - radiation effects | Carcinoma, Squamous Cell - pathology | Epithelial Cells - drug effects | Humans | Cellular Senescence - drug effects | Cell Compartmentation - radiation effects | Mucositis - prevention & control | Mouth Mucosa - drug effects | TOR Serine-Threonine Kinases - antagonists & inhibitors | Mouth Mucosa - radiation effects | Mucositis - pathology | Stem Cells - enzymology | Mucositis - enzymology | Cellular Senescence - radiation effects | Cytoprotection - drug effects | Clone Cells | Oxidative Stress - radiation effects | Cell Death - drug effects | Head and Neck Neoplasms - enzymology | Mouth Mucosa - pathology | Keratinocytes - enzymology | Superoxide Dismutase - metabolism | Radiation, Ionizing | Carcinoma, Squamous Cell - enzymology | Epithelial Cells - radiation effects | Cells, Cultured | Stem Cells - radiation effects | Epithelial Cells - pathology | Radiation Injuries - enzymology | Sirolimus - pharmacology | Head and Neck Neoplasms - pathology | Keratinocytes - pathology | Animals | Keratinocytes - drug effects | Radiation Injuries - prevention & control | Epithelial Cells - enzymology | Cell Compartmentation - drug effects | Stem Cells - drug effects | Stem Cells - pathology | Radiation Injuries - pathology | Cell Proliferation - drug effects | Mice | Oxidative Stress - drug effects | Cytoprotection - radiation effects | Cell Proliferation - radiation effects
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2. Full Text In vivo inhibition of cysteine proteases provides evidence for the involvement of 'senescence-associated vacuoles' in chloroplast protein degradation during dark-induced senescence of tobacco leaves
by Cristian A. Carrión and María Lorenza Costa and Dana E. Martínez and Christina Mohr and Klaus Humbeck and Juan J. Guiamet
Journal of Experimental Botany, ISSN 0022-0957, 1/2013, Volume 64, Issue 16, pp. 4967 - 4980
Breakdown of leaf proteins, particularly chloroplast proteins, is a massive process in senescing leaves. In spite of its importance in internal N recycling,... 
Leaves | Chloroplasts | Incubation | Cellular senescence | Botany | Plants | Plastids | Vacuoles | Chlorophylls | RESEARCH PAPER | Plant cells | Cysteine proteases | Rubisco | Senescence-associated vacuoles | Tobacco | SAG12 | Proteolysis | RIBULOSE-1,5-BISPHOSPHATE CARBOXYLASE/OXYGENASE | WHEAT TRITICUM-AESTIVUM | ARABIDOPSIS-THALIANA | NICOTIANA-TABACUM | senescence-associated vacuoles | STAY-GREEN MUTANTS | NITROGEN REMOBILIZATION | TRANSCRIPTOME ANALYSIS | PLANT SCIENCES | LEAF SENESCENCE | GENE-EXPRESSION | PHOTOSYSTEM-II | tobacco | proteolysis | Darkness | Vacuoles - enzymology | Chloroplasts - enzymology | Cellular Senescence - drug effects | Cysteine Proteases - metabolism | Down-Regulation - radiation effects | Vacuoles - drug effects | Proteolysis - drug effects | Plant Proteins - antagonists & inhibitors | Cellular Senescence - radiation effects | Chloroplasts - radiation effects | Plant Leaves - drug effects | Plant Proteins - metabolism | Chloroplasts - drug effects | Plant Leaves - enzymology | Proteolysis - radiation effects | Chloroplasts - genetics | Vacuoles - genetics | Tobacco - drug effects | Plant Leaves - radiation effects | Down-Regulation - drug effects | Tobacco - radiation effects | Plant Proteins - genetics | Vacuoles - radiation effects | Cysteine Proteases - genetics | Plant Leaves - genetics | Tobacco - genetics | Cysteine Proteinase Inhibitors - pharmacology | Tobacco - enzymology | Index Medicus
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3. Full Text Innate immune sensing of cytosolic chromatin fragments through cGAS promotes senescence
by Glück, Selene and Guey, Baptiste and Gulen, Muhammet Fatih and Wolter, Katharina and Kang, Tae-Won and Schmacke, Niklas Arndt and Bridgeman, Anne and Rehwinkel, Jan and Zender, Lars and Ablasser, Andrea
Nature Cell Biology, ISSN 1465-7392, 09/2017, Volume 19, Issue 9, pp. 1061 - 1070
Cellular senescence is triggered by various distinct stresses and characterized by a permanent cell cycle arrest. Senescent cells secrete a variety of... 
2ND-MESSENGER | DNA SENSOR | LIFE-SPAN | CELLS | CYCLIC GMP-AMP | SECRETORY PHENOTYPE | AICARDI-GOUTIERES SYNDROME | ONCOGENE-INDUCED SENESCENCE | CELLULAR SENESCENCE | CANCER | CELL BIOLOGY | Cell Proliferation | Oxidative Stress | Cytosol - immunology | Male | Cytosol - enzymology | Transfection | RNA Interference | Time Factors | Chromatin - immunology | Cellular Senescence - radiation effects | Female | Membrane Proteins - metabolism | Nucleotidyltransferases - metabolism | Paracrine Communication | Signal Transduction | Membrane Proteins - genetics | Mice, Inbred C57BL | Cells, Cultured | Genotype | Mice, Knockout | Phenotype | Animals | Chromatin - radiation effects | Nucleotidyltransferases - genetics | Chromatin - enzymology | Immunity, Innate - radiation effects | Enzyme Activation | Cytosol - radiation effects | Nucleotidyltransferases - immunology | Chromatin | Senescence | AMP | Radiation | Fragments | Paracrine signalling | Activation | Inflammation | Cyclic GMP | Cell cycle | Irradiation | Interferon | Deoxyribonucleic acid--DNA
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4. Full Text Lamin B1 loss is a senescence-associated biomarker
by Freund, Adam and Laberge, Remi-Martin and Demaria, Marco and Campisi, Judith
Molecular Biology of the Cell, ISSN 1059-1524, 06/2012, Volume 23, Issue 11, pp. 2066 - 2075
Cellular senescence is a potent tumor-suppressive mechanism that arrests cell proliferation and has been linked to aging. However, studies of senescence have... 
MOUSE DEVELOPMENT | CELLS | NUCLEAR LAMINS | DNA-DAMAGE RESPONSE | LONG-TERM EXPRESSION | GENE-EXPRESSION | TUMOR-SUPPRESSOR | CELLULAR SENESCENCE | STRUCTURAL ORGANIZATION | P53 | CELL BIOLOGY | Reactive Oxygen Species - metabolism | Humans | NF-kappa B - metabolism | RNA, Messenger - metabolism | DNA-Binding Proteins - metabolism | Cellular Senescence - radiation effects | p38 Mitogen-Activated Protein Kinases - metabolism | Signal Transduction - radiation effects | Protein-Serine-Threonine Kinases - metabolism | Radiation, Ionizing | Biomarkers - metabolism | Lamin Type B - deficiency | Cell Line | Tumor Suppressor Proteins - metabolism | RNA, Messenger - genetics | Retinoblastoma Protein - metabolism | Cell Cycle Proteins - metabolism | Tumor Suppressor Protein p53 - metabolism | Ataxia Telangiectasia Mutated Proteins | Lamin Type B - metabolism | Animals | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Gene Expression Regulation - radiation effects | Mice | DNA Damage | Dose-Response Relationship, Radiation
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5. Full Text Ionizing Radiation-Induced Endothelial Cell Senescence and Cardiovascular Diseases
by Wang, Yingying and Boerma, Marjan and Zhou, Daohong
Radiation Research, ISSN 0033-7587, 08/2016, Volume 186, Issue 2, pp. 153 - 161
Exposure to ionizing radiation induces not only apoptosis but also senescence. While the role of endothelial cell apoptosis in mediating radiation-induced... 
OXIDATIVE STRESS | ACTIVATED PROTEIN-KINASE | SECRETORY PHENOTYPE | TUMOR SUPPRESSION | DNA-DAMAGE RESPONSE | INDUCED HEART-DISEASE | BREAST-CANCER | PREMATURE SENESCENCE | BIOPHYSICS | SIGNALING PATHWAY | HEMATOPOIETIC STEM-CELLS | BIOLOGY | RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING | Cardiovascular Diseases - etiology | Animals | Endothelial Cells - cytology | Humans | Cellular Senescence - radiation effects | Endothelial Cells - radiation effects | Neoplasms - radiotherapy | Radiation Injuries - pathology | Cardiovascular Diseases - pathology | Endothelial Cells - pathology | Neoplasms - pathology | Radiation Injuries - etiology | Ionizing radiation | Causes of | Aging | Radiation injuries | Development and progression | Cardiovascular diseases | Health aspects | Apoptosis | Molecular structure | Cytokines | In vitro testing | Adhesion | Heart diseases | Endothelial cells | Vasodilation
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6. Full Text DNA-SCARS: Distinct nuclear structures that sustain damage-induced senescence growth arrest and inflammatory cytokine secretion
by Rodier, Francis and Muñoz, Denise P and Teachenor, Robert and Chu, Victoria and Le, Oanh and Bhaumik, Dipa and Coppé, Jean-Philippe and Campeau, Eric and Beauséjour, Christian M and Kim, Sahn-Ho and Davalos, Albert R and Campisi, Judith
Journal of Cell Science, ISSN 0021-9533, 01/2011, Volume 124, Issue 1, pp. 68 - 81
DNA damage can induce a tumor suppressive response termed cellular senescence. Damaged senescent cells permanently arrest growth, secrete inflammatory... 
Interleukin 6 (IL6) | Homologous recombination | Cellular senescence | Aging | Promyelocytic leukemia protein (PML) | DNA repair | Cancer | HUMAN-CELLS | TRIGGERS SENESCENCE | HUMAN TELOMERES | DOUBLE-STRAND BREAKS | ONCOGENE-INDUCED SENESCENCE | CELL BIOLOGY | PREMATURE SENESCENCE | IN-VIVO | HUMAN FIBROBLASTS | AGING PRIMATES | Cell Line | Chromatin - metabolism | Tumor Suppressor Proteins - metabolism | Cytokines - metabolism | Cell Cycle - radiation effects | Humans | Mice, Inbred C57BL | Nuclear Proteins - metabolism | Transcription Factors - genetics | Transcription Factors - metabolism | Animals | Cell Nucleus - metabolism | Cell Nucleus - genetics | Cell Nucleus - radiation effects | X-Rays | Tumor Suppressor Proteins - genetics | Cellular Senescence - radiation effects | Mice | Histones - metabolism | Nuclear Proteins - genetics | Chromatin - genetics | Cytokines - genetics | DNA Damage - radiation effects | Promyelocytic Leukemia Protein
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7. Full Text Radiation-induced accelerated senescence
: A fate worse than death?
by Day, Regina M and Snow, Andrew L and Panganiban, Ronald Allan M
Cell Cycle, ISSN 1538-4101, 07/2014, Volume 13, Issue 13, pp. 2011 - 2012
MECHANISMS | CELLULAR SENESCENCE | ENDOTHELIAL-CELLS | CELL BIOLOGY | Cellular Senescence - drug effects | Receptor, IGF Type 1 - antagonists & inhibitors | Endothelial Cells - cytology | Humans | Cellular Senescence - radiation effects
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8. Full Text Accelerated senescence: An emerging role in tumor cell response to chemotherapy and radiation
by Gewirtz, David A and Holt, Shawn E and Elmore, Lynne W
Biochemical Pharmacology, ISSN 0006-2952, 2008, Volume 76, Issue 8, pp. 947 - 957
Treatment of malignancies with chemotherapeutic drugs and/or radiotherapy is designed to eliminate the disease by depriving the tumor cell of its reproductive... 
Chemotherapy | Radiation | Replicative senescence | Accelerated senescence | Telomere | Telomerase | p21 | cdc2 | p53 | TERMINAL GROWTH ARREST | DNA-DAMAGE | DOUBLE-STRAND BREAKS | LUNG-CANCER CELLS | NORMAL HUMAN FIBROBLASTS | TOPOISOMERASE-I INHIBITION | TELOMERASE ACTIVITY | PHARMACOLOGY & PHARMACY | IONIZING-RADIATION | ADRIAMYCIN-INDUCED SENESCENCE | Humans | Cell Division - radiation effects | Cellular Senescence - drug effects | Antineoplastic Agents - therapeutic use | Telomere - drug effects | Cell Division - drug effects | Neoplasms - drug therapy | Telomere - radiation effects | Cisplatin - therapeutic use | Signal Transduction - drug effects | Cellular Senescence - radiation effects | Cell Line, Tumor | Neoplasms - radiotherapy | Neoplasms - physiopathology | Signal Transduction - radiation effects | DNA Damage - radiation effects | Radiation, Ionizing
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9. Full Text Molecular mechanisms of UVB-induced senescence of dermal fibroblasts and its relevance for photoaging of the human skin
by Cavinato, Maria and Jansen-Dürr, Pidder
Experimental Gerontology, ISSN 0531-5565, 08/2017, Volume 94, pp. 78 - 82
Due to its ability to cross the epidermis and reach the upper dermis where it causes cumulative DNA damage and increased oxidative stress, UVB is considered... 
UVB | Fibroblasts | Skin aging | Photoaging | Autophagy | Proteasome | IRRADIATION | STRESS-RESPONSE | PHOTOCARCINOGENESIS | CELL | GERIATRICS & GERONTOLOGY | Autophagy - radiation effects | Skin - metabolism | Humans | Skin Aging - radiation effects | Fibroblasts - pathology | Ultraviolet Rays - adverse effects | Fibroblasts - radiation effects | Signal Transduction - drug effects | Proteolysis | Skin - radiation effects | Cellular Senescence - radiation effects | Oxidative Stress - radiation effects | DNA Damage | Proteasome Endopeptidase Complex - metabolism | Proteasome Endopeptidase Complex - radiation effects | Skin - pathology | Fibroblasts - metabolism | Analysis | Skin
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10. Full Text Quantitative proteomic analysis reveals induction of premature senescence in human umbilical vein endothelial cells exposed to chronic low‐dose rate gamma radiation
by Yentrapalli, Ramesh and Azimzadeh, Omid and Barjaktarovic, Zarko and Sarioglu, Hakan and Wojcik, Andrzej and Harms‐Ringdahl, Mats and Atkinson, Michael J and Haghdoost, Siamak and Tapio, Soile and Stockholms universitet and Naturvetenskapliga fakulteten and Institutionen för genetik, mikrobiologi och toxikologi
PROTEOMICS, ISSN 1615-9853, 04/2013, Volume 13, Issue 7, pp. 1096 - 1107
Chronic low‐dose ionizing radiation induces cardiovascular disease in human populations but the mechanism is largely unknown. We suggested that chronic... 
Cell biology | Ionizing radiation | Senescence | ICPL | Endothelium | MORTALITY EXPERIENCE | LIFE-SPAN | ERM PROTEINS | BIOCHEMISTRY & MOLECULAR BIOLOGY | BIOCHEMICAL RESEARCH METHODS | FACTOR MIF | EARLY-PASSAGE | PLASMINOGEN-ACTIVATOR INHIBITOR | REPLICATIVE SENESCENCE | CHERNOBYL EMERGENCY WORKERS | APOE(-/-) MICE | IONIZING-RADIATION | Gamma Rays | Reproducibility of Results | Human Umbilical Vein Endothelial Cells - metabolism | Humans | Tumor Suppressor Protein p53 - metabolism | Immunoblotting | Cell Shape - radiation effects | Human Umbilical Vein Endothelial Cells - cytology | Cellular Senescence - radiation effects | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Proteomics - methods | Signal Transduction - radiation effects | Human Umbilical Vein Endothelial Cells - radiation effects | Dose-Response Relationship, Radiation | Metabolic Networks and Pathways - radiation effects | Proteome - metabolism | Cell Proliferation - radiation effects | Gamma rays | Cellular proteins | Nuclear radiation | Analysis | Labeling-machines | Cells | Proteins | Cellular biology | Radiation | Biological Sciences | Naturvetenskap | Biokemi och molekylärbiologi | Biologiska vetenskaper | Biochemistry and Molecular Biology | Natural Sciences
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11. Full Text Pluripotent stem cells escape from senescence-associated DNA methylation changes
by Koch, CM and Reck, K and Shao, KF and Lin, Q and Joussen, S and Ziegler, P and Walenda, G and Drescher, W and Opalka, B and May, T and Brummendorf, T and Zenke, M and Saric, T and Wagner, W
GENOME RESEARCH, ISSN 1088-9051, 02/2013, Volume 23, Issue 2, pp. 248 - 259
Pluripotent stem cells evade replicative senescence, whereas other primary cells lose their proliferation and differentiation potential after a limited number... 
DEFINED FACTORS | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELLULAR SENESCENCE | CANCER | REPLICATIVE SENESCENCE | MESENCHYMAL STROMAL CELLS | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | CPG SITES | GENETICS & HEREDITY | GENE-EXPRESSION | HUMAN FIBROBLASTS | HETEROCHROMATIN FORMATION | TELOMERE LENGTH | Cellular Senescence - genetics | Mesenchymal Stromal Cells - radiation effects | Gamma Rays - adverse effects | Humans | Middle Aged | Cells, Cultured | Mesenchymal Stromal Cells - metabolism | Epigenesis, Genetic - radiation effects | Induced Pluripotent Stem Cells - radiation effects | Pluripotent Stem Cells - metabolism | DNA Methylation - radiation effects | Models, Biological | Cellular Senescence - radiation effects | Adult | Pluripotent Stem Cells - radiation effects | Aged | Cell Line, Transformed | Induced Pluripotent Stem Cells - metabolism | Cell proliferation | Gene targeting | Stem cells | Physiological aspects | Genetic aspects | Research | Cell differentiation | Gene expression
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