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Hillblom Chemical Biology of Aging Network
Hillblom Chemical Biology of Aging Network is an effort led by the scientists at the Buck Institute to screen as many as 120,000 chemical compounds to discover which ones impact human lifespan.These compounds are researched in four research models – yeast, nematode worms, fruit flies and mice and the results will be most likely made public sometime during 2009-2010. The research network is being funded by the Larry L. Hillblom Foundation. The idea of the research is to find "needles in the haystack", or, in other words, find new starting points for experiments based on compounds that have never been considered as candidates for lifespan extension. The style of the research is that of an inverted pyramid. The largest number of compounds will be screened, in many cases via the use of robotics and other high-tech devices, in the simplest organisms (budding yeast and nematode worms). Those chemicals that do extend lifespan in those species will go on to be tested in the fruit fly. Chemicals that cause all three species to live longer will be looked at in mice models. Mice share about 85% of their genetic make up with Homo sapiens. The Buck Institute, which is the leading institute in the research, is located in Novato, California, and is solely devoted to the basic research on aging and age-associated diseases. Hillblom Chemical Biology of Aging Network - Related StudiesKapahi, P., Zid, B. M., Harper, T., Koslover, D., Sapin, V., and Benzer, S. 2004. Regulation of lifespan in Drosophila by modulation of genes in the TOR signaling pathway. Curr Biol 14:885–890. Kapahi, P. and Zid, B. 2004. TOR Pathway: Linking Nutrient Sensing to Life Span. Sci Aging Knowl Environ 36:34. Beausejour, C. M., Krtolica, A., Galimi, F., Narita, M., Lowe, S. W., Yaswen, P., and Campisi, J. 2003. Reversal of human cellular senescence: roles of the p53 and p16 pathways. Embo J22:4212–4222. Busuttil, R. A., Rubio, M., Dolle, M. E., Campisi, J., and Vijg, J. 2003. Oxygen accelerates the accumulation of mutations during the senescence and immortalization of murine cells in culture. Aging Cell 2:287–294. Chen, L. J., Huang, S., Lee, L., Davalos, A., Schiestl, R. H., Campisi, J., and Oshima, J. 2003. WRN, the protein deficient in Werner syndrome, plays a critical structural role in optimizing DNA repair. Aging Cell 2:191–199. Chiang, J., Hatchcock, K., Kim, S. H., Campisi, J., and Hodes, R. 2004. Telomere associated protein TIN2 is essential for early embryonic development through a telomerase independent pathway. Molec Cell Biol 24:6631–6634. Davalos, A. R. and Campisi, J. 2003. Bloom syndrome cells undergo p53-dependent apoptosis and delayed assembly of BRCA1 and NBS1 repair complexes at stalled replication forks. J Cell Biol 162:1197–1209. Kim, S. H., Beausejour, C., Davalos, A. R., Kaminker, P., Heo, S. J., and Campisi, J. 2004. TIN2 mediates functions of TRF2 at human telomeres. J Biol Chem 279:43799–43804. Parrinello, S., Samper, E., Krtolica, A., Goldstein, J., Melov, S., and Campisi, J. 2003. Oxygen sensitivity severely limits the replicative lifespan of murine fibroblasts. Nat Cell Biol 5:741–747. Rubio, M., Davalos, A., and Campisi, J. 2004. Telomere length regulates the effects of telomerase on the cellular response to genotoxic stress. Exp Cell Res 298:17–27.
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