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I demonstrate that HAT p300 acetylates MYC preferentially at K157/158 in transfected mammalian cells. I also show that MYC overexpression increases the level of endogenous p300. Moreover, our data provides a potential link between MYC acetylation and its biological functions. I found that MYC acetylation at lysine 158 reduces MYC-activated apoptosis and this could be via transcriptional regulation of pro-apoptotic Nrf1 and Cytochrome c (Cyc) genes. These findings might be important for prospective drug development against MYC-dependent tumors. New therapeutics which drive transformed cells to…mehr

Produktbeschreibung
I demonstrate that HAT p300 acetylates MYC preferentially at K157/158 in transfected mammalian cells. I also show that MYC overexpression increases the level of endogenous p300. Moreover, our data provides a potential link between MYC acetylation and its biological functions. I found that MYC acetylation at lysine 158 reduces MYC-activated apoptosis and this could be via transcriptional regulation of pro-apoptotic Nrf1 and Cytochrome c (Cyc) genes. These findings might be important for prospective drug development against MYC-dependent tumors. New therapeutics which drive transformed cells to apoptosis via prevention of MYC acetylation at K157/158 by p300 could be beneficial for the treatment of MYC-dependent cancers.
Autorenporträt
Marina Vorontchikhina received her M.D. from Russian State Medical University and Ph.D. in Cell, Molecular and Developmental Biology from University of California (UCR, Dr. Martinez laboratory). She did her postdoctoral training with Dr. Kitajewski at Columbia University (New York, USA) and Dr. Tlsty at University of California (UCSF).