ATR promotes mTORC1 activation via de novo cholesterol synthesis in p16-low cancer cells
Naveen Kumar Tangudu,
Zhentai Huang,
Richard Fang
et al.
Abstract:DNA damage and cellular metabolism are intricately linked with bidirectional feedback. Two of the main effectors of the DNA damage response and control of cellular metabolism are ATR and mTORC1, respectively. Prior work has placed ATR upstream of mTORC1 during replication stress, yet the direct mechanism for how mTORC1 is activated in this context remain unclear. We previously published that p16-low cells have mTORC1 hyperactivation, which in part promotes their proliferation. Using this model, we found that A… Show more
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