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Senescence, cell

Riou JF et al. (2002) Cell senescence and telomere shortening induced by a new series of speciflc G-quadruplex DNA ligands. Proc Natl Acad Sci USA 99(5) 2672-2677... [Pg.95]

There are two major classes of freshwater cyanobacterial toxins, broadly categorized according to their physiological effects on vertebrates hepatotoxins and neurotoxins. Although these hydrophilic toxins are highly soluble, they are typically released only upon cell lysis following mechanical damage or cell senescence (Sivonen and Jones 1999). [Pg.107]

DMSP. DMSP and related sulfur compounds generated by planktonic microalgae are involved in a complex series of interactions and reactions that occur in seawater and the atmosphere (Malin et al. 1992 Liss et al. 1994 Malin 1996 Malin and Kirst 1997 Steinke et al. 2002 Yoch 2002). In the oceans, DMS can originate from DMSP that is cleaved during grazing, be directly released by healthy algal cells, or be released when cells senesce or are lysed by viruses (Fig. 8.3). [Pg.186]

The mechanistic basis of the anti-neoplastic activity of UDCA and the explanation for the significant difference in bioactivity of UDCA compared with DCA despite marked similarity in chemical structure remain unresolved. UDCA administration in healthy volunteers and colorectal adenoma patients has been demonstrated to decrease the proportion of DCA in aqueous phase stool. Therefore, one possible mechanism of the chemopreventative activity of UDCA is reduction of mucosal secondary bile acid exposure. Consistent with this idea, UDCA administration has been demonstrated to reduce the incidence of K-ras mutations and decrease Cox-2 expression in AOM-induced tumors, which is the opposite of the reported effects of DCA in the same model. However, it is clear that exogenous administration of UDCA has direct anti-neoplastic activity on human CRC cells in vitro, either alone or in combination with DCA, including anti-proliferative and anti-apoptotic effects, as well as induction of cell senescence. " ... [Pg.92]

Serrano M, Lin AW, MeCurraeh ME et al. Oncogenic ras provokes premature cell senescence associated with aecumulation ofp53 and pl6INK4a. Cell 1997 88 593-602. [Pg.124]

Furthermore, Ang n has been found to contribute to VSMC senescence, which has been implicated in the pathogenesis of atherosclerosis (Kunieda et al. 2006). Cell senescence may promote plaque instability, since loss of VSMCs leads to transformation into a rupture-prone plaque with a thin fibrous cap over the lipid-rich core (Geng and Libby 2002). [Pg.107]

Xia, L., Wang, X.X., Hu, X.S., Guo, X.G., Shang, Y.P., Chen, H.J., Zeng, C.L., Zhang, F.R., Chen, J.Z. (2008). Resveratrol reduces endothelial progenitor cells senescence through augmentation of telomerase activity by Akt-dependent mechanisms. Br. J. Pharmacol. June 30. (Epub ahead of print)... [Pg.92]

V. Urquidi, D. Tarin, and S. Goodison. 2000. Role of telomerase in cell senescence and oncogenesis Annu. Rev. Med. 51 65-79. (PubMed)... [Pg.1157]

The 9-anilino proflavine derivative was designed to optimize the interaction with the intramolecular G-quadruplex from human telomere and minimize that with duplex DNA. These compounds have 60 to 100 nM potency in a modified TRAP assay and corresponding low cytotoxicity (93). The triazines have been demonstrated to produce telomere shortening, which is associated with delayed growth arrest and cell senescence (80). The fluoroquinophenoxazines are redesigned topoisomerase II poisons that now interact more specifically with G-quadruplex structures, and this activity is correlated with production of anaphase bridges (78), a property also shared by the cationic porphyrin TMPyP4 (96) and... [Pg.372]

Mountz JD, Wu J, Zhou T, Hsu H-C. Cell death and longevity implications of Pas-mediated apoptosis in T-cell senescence. Immunol Rev 1997 160 19-30. [Pg.94]


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