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Baena, E. et al.

c-Myc regulates cell size and ploidy but is not essential for postnatal proliferation in liver.

The c-Myc protein is a transcription factor implicated in the regulation of multiple biological processes, including cell proliferation, cell growth, and apoptosis. In vivo overexpression of c-myc is linked to tumor development in a number of mouse models. Here, we show that perinatal inactivation of c-Myc in liver causes disorganized organ architecture, decreased hepatocyte size, and cell ploidy. Furthermore, c-Myc appears to have distinct roles in proliferation in liver. Thus, postnatal hepatocyte proliferation does not require c-Myc, whereas it is necessary for liver regeneration in adult mice. These results show novel physiological functions of c-myc in liver development and hepatocyte proliferation and growth.[1]

References

c-Myc regulates cell size and ploidy but is not essential for postnatal proliferation in liver. Baena, E., Gandarillas, A., Vallespinós, M., Zanet, J., Bachs, O., Redondo, C., Fabregat, I., Martinez-A, C., de Alborán, I.M. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]

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