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Titlebook: Aging of Cells in and Outside the Body; Sunil C. Kaul,Renu Wadhwa Book 2003 Springer Science+Business Media Dordrecht 2003 Chaperone.aging

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楼主: Interpolate
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The p53 Pathway, Cancer and Aging,self, or defects in its regulation, are probably the most common genetic markers of all human cancers [1]. Despite the fact that tumor etiologies differ widely, this evidence shows that there are common pathways in tumor development. A key step in tumor development is the conversion of a cell from o
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Regulation of Cellular Senescence by the Retinoblastoma Pathway,ly exponential kinetics and eventually reach a state of permanent growth arrest, referred to as replicative senescence [1]. Senescent cells remain viable and metabolically active, but cannot re-initiate DNA replication in response to physiological mitogenic stimuli [1–3]. Expression of .enescence-.s
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Therapeutic Induction of Cellular Senescence: Nuclear Matrix in Senescence,is featured most typically by specific morphological alterations, flat and enlarged cell shape, and induction of senescence markers such as fibronectin, collagenase I, and senescence-associated β-galactosidase [2]. It is also shown that in normally senesced human fibroblasts the cyclin-dependent pro
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Use of Hammerhead Ribozymes for Aging and Cancer,scades (replication, transcription and translation) by catalyzing essential steps such as cleavage and ligation [2]. Hammerhead ribozymes (for resemblance of their two-dimensional structure to a hammerhead) are the smallest ribozymes that are used as molecular scissors in molecular biology and biote
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Özge Yaren Türkseven,Orhan Gündüz,Alper Babaoblasts, epithelial cells, endothelial cells, keratinocytes, melanocytes, chondrocytes, muscle satellite cells, articular cartilage cells, glial cells, lymphocytes, trabecular osteoblasts and bone marrow cells, isolated from a variety of tissues and animals.
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Cultural Heritage and Resilience,s that a direct correlation exists between species life span and . life span [2], but that this correlation is inverse with donorage [3–7]. The frequency of reversal of the senescence phenotype (i.e., immortalization) varies greatly with different animal species. The probability of immortalization (
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