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Molecular Cell 22, 129 136, April 7, 2006 2006 Elsevier Inc. DOI 10.1016/j.molcel.2006.03.011 AGO1 Homeostasis Entails Short Article Coexpression of MIR168 and AGO1 and Preferential Stabilization

MA 02138 United States Corresponding Author. E-mail: barchartdgmail.com Abstract In this paper we discuss recent results in which our laboratory has identified a key function of mTORC1 in the regulation of G0/G1 cell cycle progression, and highlight the potential of targeted motor inhibitors that can reverse the regulation by restoring its normal function. The role of motor in developmental and adult aging Human aging represents a dynamic process that is affected by both genetic and environmental factors. The process occurs by a coordinated cascade of effects that are initiated by changes in transcriptional reprogramming and/or regulation or modification of translation initiation factors, in response to the accumulation of DNA damage and/or to the activation of the transcription factors that promote the transcription of cellular genes (Swan et al., 2005). These transcriptional changes can result in an imbalance between the accumulation of mRNAs and the repression of the production of proteins. These two processes are characterized in the aging process by mTORC1 (mammalian target of kanamycin; Miller et al., 2005), a protein complex consisting of the motor (target of kanamycin) and GATA1 (growth and adapting; Reimburse and Aiken's, 2005). As mTORC1 is required for the phosphorylation of ribosomal factors and for stabilization of the transcription factor complex, we have previously used mTORC1 in our in silicon model to explain age-related cellular processes (Reimburse et al., 2007). These models have provided experimental evidence that mTORC1 is a key mediator of the process of cellular aging (Brass et al., 2004) and that mTORC1 activation is essential for growth and for the maintenance of mitotic and postmitotic stages of cell division. Recent evidence has demonstrated the role of mTORC1 and AGO1 in cell cycle progression, thus underscoring the importance of the processes of mTORC1-AGO1 regulation in the regulation of G0/G1 cell cycle progression in vivo. For example, in cultured mammalian cells, over expression of mTORC1 results in reduced mitotic potential and increased apoptosis (Zhang et al., 2008). Likewise, in S phase rat hepatocytes, inhibition of motor activation decreases both the degree of mitotic arrest (Tsuchiguchi et al., 2007) and the cell size (Tsuchiguchi et al.

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