Abstract
Senescent cells alter their microenvironment by secreting a growing collection of factors, a phenomenon termed the senescence-associated secretory phenotype (SASP). Cellular senescence is often the result of nuclear DNA damage fuelling a chronic DNA damage response (DDR). Upstream elements of the DDR cascade are necessary for full blown SASP, and additional crosstalk occurs between the DDR and cytokine secretion.
MeSH terms
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Ataxia Telangiectasia Mutated Proteins
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Cell Cycle Proteins / genetics
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Cell Cycle Proteins / metabolism
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Cells, Cultured
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Cellular Senescence / physiology*
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Checkpoint Kinase 2
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Cytokines / metabolism*
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DNA Damage*
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / metabolism
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Fibroblasts / cytology
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Fibroblasts / metabolism
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Fibroblasts / radiation effects
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Humans
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Interleukin-6 / metabolism
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Male
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Models, Biological
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Nuclear Proteins / genetics
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Nuclear Proteins / metabolism
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Protein Serine-Threonine Kinases / genetics
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Protein Serine-Threonine Kinases / metabolism
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RNA, Small Interfering / genetics
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Signal Transduction / physiology*
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Transfection
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Tumor Suppressor Proteins / genetics
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Tumor Suppressor Proteins / metabolism
Substances
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Cell Cycle Proteins
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Cytokines
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DNA-Binding Proteins
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Interleukin-6
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NBN protein, human
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Nuclear Proteins
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RNA, Small Interfering
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Tumor Suppressor Proteins
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Checkpoint Kinase 2
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ATM protein, human
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Ataxia Telangiectasia Mutated Proteins
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CHEK2 protein, human
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Protein Serine-Threonine Kinases