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Cellular senescence

Senescence is defined as cellular ageing resulting in an irreversible cell cycle arrest. Primary cells divide about 50 times and then are arrested due to senescence. Senescence is associated with shortening of telomeres. [Pg.1118]

Within the plant. Excessive concentrations of some ions occur in the tissue overall, in the cytoplasm, or in the apoplast. Effects include metabolic inhibition, interference with protein synthesis, cellular dehydration, stomatal closure and early senescence of leaves. Since both cytoplasm and apoplast are small compartments, imbalance between compartments may amplify the effects of excess salt, resulting in toxicity despite apparently moderate overall tissue concentrations. [Pg.221]

The maintenance of cellular homeostasis involves a balance of cell division, differentiation, senescence, and apoptosis. [Pg.1426]

In allelopathy studies, the allelochemicals first influence the physiological and biochemical processes in cells. Till now there is no book of methods to study allelopathic interactions in the cells. The activity of cells influence various important physiological processes like seed germination, plant growth and development, photosynthesis and respiration, senescence and abscission are included in this volume. To understand the basic mechanisms of various physiological processes, being affected by allelochemicals at the cellular level enzyme activity and metabolite studies are essential. [Pg.8]

When the light microscope (LM) alone is not sufficient to study a system, the binding of an electron-dense ligand to an antibody facilitates the use of an EM. There are times when, in addition to EM study, immunoelectron microscopic analysis is necessary. Observed anatomical changes often lead to inquiries on the molecular events. This proved true in the case of the report by Inada et al. (22) in which they described a three-dimensional analysis of the senescence program in rice (Oryza sativa L.) coleoptiles. Immunoelectron microscopy was used to determine the behavior of cellular DNA during senescence. The procedure employed by the investigators is detailed below. [Pg.296]

Langley, E., et al.. Human SIR2 deacetylates p53 and antagonizes PML/p53-induced cellular senescence. Embo J, 2002, 21(10), 2383-96. [Pg.90]

DNA-PK Homo sapiens Breast cancer downregulated during cellular senescence PARP, SAF-A... [Pg.216]

Fibroblast APOE levels increase under conditions of serum-starvation-induced growth arrest and hypoxia-induced senescence. In both cases, increased nuclear APOE levels are observed, particularly in cells that accumulate lipofuscin. Nuclear APOE is translocated to the cytosol when mitotic nuclear disassembly occurs, and this is associated with an increase in total cellular APOE levels (500). [Pg.297]

Chronic injury results primarily from secondary reactions involving membrane injury. The oxidants could cause the formation of free radicals or other, more stable oxidants (such as hydrogen peroxide), which in turn could cause secondary reactions. These secondary reactions could stimulate the production of cellular ethylene, with tissue senescence re suiting. These secondary reactions may predispose plants to increased injury from later acute exposures by limiting their repair capability. This predisposition concept has been noted in several reports. [Pg.459]

The cell lines employed differ in many aspects from normal body cells. Human cells taken from normal tissue and maintained in primary culture with the addition of suitable nutrient media only have a limited capacity for division. Cells of primary cultures of human fibroblasts, for example, halt cell division activity after 50—60 cell divisions and enter a state known as cellular senescence. In contrast, cells taken from a tumor often have an imlimited ability to divide in cell culture. [Pg.427]

Thus, the genome goes from the incipient state to childhood, adult life, senescence, and death, and as it does it expresses itself in different forms. Childhood would be the time when the genetic mechanisms develop, and adulthood would result in an escape from the single cellular state to the production of animals and plants. Genomic senescence (the absolute energy valley) may be an inescapable phenomenon that will eventually lead to the extinction of species. [Pg.55]


See other pages where Cellular senescence is mentioned: [Pg.33]    [Pg.413]    [Pg.449]    [Pg.6]    [Pg.208]    [Pg.1278]    [Pg.120]    [Pg.214]    [Pg.229]    [Pg.223]    [Pg.440]    [Pg.233]    [Pg.220]    [Pg.617]    [Pg.236]    [Pg.294]    [Pg.303]    [Pg.308]    [Pg.442]    [Pg.686]    [Pg.164]    [Pg.166]    [Pg.99]    [Pg.101]    [Pg.108]    [Pg.116]    [Pg.11]    [Pg.1027]    [Pg.405]    [Pg.510]    [Pg.656]    [Pg.33]    [Pg.346]    [Pg.86]    [Pg.251]    [Pg.556]    [Pg.462]    [Pg.462]   
See also in sourсe #XX -- [ Pg.1278 ]

See also in sourсe #XX -- [ Pg.427 ]




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