Sat, 19 Jul 2008 01:26:03 BST CiteULike: jyuh's Morimura http://www.citeulike.org/user/jyuh/author/Morimura CiteULike.org en-gb Copyright © 2004-2008 citeulike.org http://www.citeulike.org/user/jyuh/article/2354122 <i>Cell, Vol. 132, No. 3. (8 February 2008), pp. 487-498.</i><br /><br />Summary The cell-cycle transition from G1 to S phase has been difficult to visualize. We have harnessed antiphase oscillating proteins that mark cell-cycle transitions in order to develop genetically encoded fluorescent probes for this purpose. These probes effectively label individual G1 phase nuclei red and those in S/G2/M phases green. We were able to generate cultured cells and transgenic mice constitutively expressing the cell-cycle probes, in which every cell nucleus exhibits either red or green fluorescence. We performed time-lapse imaging to explore the spatiotemporal patterns of cell-cycle dynamics during the epithelial-mesenchymal transition of cultured cells, the migration and differentiation of neural progenitors in brain slices, and the development of tumors across blood vessels in live mice. These mice and cell lines will serve as model systems permitting unprecedented spatial and temporal resolution to help us better understand how the cell cycle is coordinated with various biological events. Visualizing Spatiotemporal Dynamics of Multicellular Cell-Cycle Progression Asako Sakaue-Sawano Hiroshi Kurokawa Toshifumi Morimura Aki Hanyu Hiroshi Hama Hatsuki Osawa Saori Kashiwagi Kiyoko Fukami Takaki Miyata Hiroyuki Miyoshi Takeshi Imamura Masaharu Ogawa Hisao Masai Atsushi Miyawaki doi:10.1016/j.cell.2007.12.033 Cell, Vol. 132, No. 3. (8 February 2008), pp. 487-498. 2008-02-08T16:32:00-00:00 2008 Cell 132 3 487 498 no-tag http://www.citeulike.org/user/jyuh/article/1971455 <i>Carcinogenesis, Vol. 26, No. 11. (November 2005), pp. 1835-1845.</i><br /><br />Recently the idea of hormesis, a biphasic dose-response relationship in which a chemical exerts opposite effects dependent on the dose, has attracted interest in the field of carcinogenesis. With non-genotoxic agents there is considerable experimental evidence in support of hormesis and the present review highlights current knowledge of dose-response effects. In particular, several in vivo studies have provided support for the idea that non-genotoxic carcinogens may inhibit hepatocarcinogenesis at low doses. Here, we survey the examples and discuss possible mechanisms of hormesis using phenobarbital, 1,1-bis(p-chlorophenyl)-2,2,2-trichloroethane (DDT), alpha-benzene hexachloride (alpha-BHC) and other non-genotoxins. Furthermore, the effects of low and high doses of non-genotoxic and genotoxic compounds on carcinogenesis are compared, with especial attention to differences in mechanisms of action in animals and possible application of the dose-response concept to cancer risk assessment in humans. Epigenetic processes differentially can be affected by agents that impinge on oxidative stress, DNA repair, cell proliferation, apoptosis, intracellular communication and cell signaling. Non-genotoxic carcinogens may target nuclear receptors, cause aberrant DNA methylation at the genomic level and induce post-translational modifications at the protein level, thereby impacting on the stability or activity of key regulatory proteins, including oncoproteins and tumor suppressor proteins. Genotoxic agents, in contrast, cause genetic change by directly attacking DNA and inducing mutations, in addition to temporarily modulating the gene activity. Carcinogens can elicit a variety of changes via multiple genetic and epigenetic lesions, contributing to cellular carcinogenesis. Hormesis and dose-response-mediated mechanisms in carcinogenesis: evidence for a threshold in carcinogenicity of non-genotoxic carcinogens. S Fukushima A Kinoshita R Puatanachokchai M Kushida H Wanibuchi K Morimura Carcinogenesis, Vol. 26, No. 11. (November 2005), pp. 1835-1845. 2007-11-24T09:50:28-00:00 2005 Carcinogenesis 0143-3334 26 11 1835 1845 no-tag