共查询到20条相似文献,搜索用时 0 毫秒
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Molecular cloning of rat transcription factor YY1 总被引:1,自引:0,他引:1
Nishiyama C Yokota T Nishiyama M Ra C Okumura K Ogawa H 《Bioscience, biotechnology, and biochemistry》2003,67(3):654-658
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YY1 functions with INO80 to activate transcription 总被引:1,自引:0,他引:1
Cai Y Jin J Yao T Gottschalk AJ Swanson SK Wu S Shi Y Washburn MP Florens L Conaway RC Conaway JW 《Nature structural & molecular biology》2007,14(9):872-874
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Reversal of human cellular senescence: roles of the p53 and p16 pathways 总被引:34,自引:0,他引:34
Beauséjour CM Krtolica A Galimi F Narita M Lowe SW Yaswen P Campisi J 《The EMBO journal》2003,22(16):4212-4222
Telomere erosion and subsequent dysfunction limits the proliferation of normal human cells by a process termed replicative senescence. Replicative senescence is thought to suppress tumorigenesis by establishing an essentially irreversible growth arrest that requires activities of the p53 and pRB tumor suppressor proteins. We show that, depending on expression of the pRB regulator p16, replicative senescence is not necessarily irreversible. We used lentiviruses to express specific viral and cellular proteins in senescent human fibroblasts and mammary epithelial cells. Expression of telomerase did not reverse the senescence arrest. However, cells with low levels of p16 at senescence resumed robust growth upon p53 inactivation, and limited growth upon expression of oncogenic RAS. In contrast, cells with high levels of p16 at senescence failed to proliferate upon p53 inactivation or RAS expression, although they re-entered the cell cycle without growth after pRB inactivation. Our results indicate that the senescence response to telomere dysfunction is reversible and is maintained primarily by p53. However, p16 provides a dominant second barrier to the unlimited growth of human cells. 相似文献
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Mina Sasaki Hiroshi Kajiya Satoru Ozeki Koji Okabe Tetsuro Ikebe 《Biochemical and biophysical research communications》2014
Reactive oxygen species (ROS) can cause severe damage to DNA, proteins and lipids in normal cells, contributing to carcinogenesis and various pathological conditions. While cellular senescence arrests the early phase of cell cycle without any detectable telomere loss or dysfunction. ROS is reported to contribute to induction of cellular senescence, as evidence by its premature onset upon treatment with antioxidants or inhibitors of cellular oxidant scavengers. Although cellular senescence is known to be implicated in tumor suppression, it remains unknown whether ROS initially contributed to be cellular senescence in normal human epidermal keratinocytes (NHEK) and their malignant counterparts. To clarify whether ROS induce cellular senescence in NHEKs, we examined the effect of hydrogen peroxide (H2O2) on the expression of cellular senescence-associated molecules in NHEKs, compared to in squamous carcinoma cells (SCCs). Hydrogen peroxide increased the number of cells positive in senescence associated-β-galactosidase (SA-β-Gal) activity in NHEKs, but not SCCs. The expression of cyclin-dependent kinase (CDK) inhibitors, especially p16INK4a was upregulated in NHEKs treated with H2O2. Interestingly, H2O2 suppressed the methylation of p16INK4a, promoter region in NHEKs, but not in SCCs. Hydrogen peroxide also suppressed the expression of phosphorylated Rb and CDK4, resulting in arrest in G0/G1 phase in NHEKs, but not SCCs. 相似文献
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