P53/TAp63 and AKT regulate mammalian target of rapamycin complex 1 (mTORC1) signaling through two independent parallel pathways in the presence of DNA damage

Maren Cam; Hemant K. Bid; Linlin Xiao; Gerard P. Zambetti; Peter J. Houghton; Hakan Cam

doi:10.1074/jbc.M113.530303

P53/TAp63 and AKT regulate mammalian target of rapamycin complex 1 (mTORC1) signaling through two independent parallel pathways in the presence of DNA damage

Maren Cam, Hemant K. Bid, Linlin Xiao, Gerard P. Zambetti, Peter J. Houghton, Hakan Cam

Research output: Contribution to journal › Article › peer-review

40 Scopus citations

Abstract

Background: mTORC1 integrates cellular inputs and is often deregulated in cancer. Results: In response to DNA damage, p53/TAp63 and AKT regulate mTORC1 through two independent parallel pathways. Conclusion: DNA damage activates Akt, resulting in inhibition of S6K1, whereas Sestrin1/2 downstream of p53 and REDD1 downstream of p63 coordinate to suppress 4E-BP1. Significance: mTORC1-dependent 4EBP1 inhibition by DNA damage is abrogated in most human cancers.

Original language	English (US)
Pages (from-to)	4083-4094
Number of pages	12
Journal	Journal of Biological Chemistry
Volume	289
Issue number	7
DOIs	https://doi.org/10.1074/jbc.M113.530303
State	Published - Feb 14 2014
Externally published	Yes

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Cell Biology

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P53/TAp63 and AKT regulate mammalian target of rapamycin complex 1 (mTORC1) signaling through two independent parallel pathways in the presence of DNA damage. / Cam, Maren; Bid, Hemant K.; Xiao, Linlin; Zambetti, Gerard P.; Houghton, Peter J.; Cam, Hakan.

In: Journal of Biological Chemistry, Vol. 289, No. 7, 14.02.2014, p. 4083-4094.

Research output: Contribution to journal › Article › peer-review

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abstract = "Background: mTORC1 integrates cellular inputs and is often deregulated in cancer. Results: In response to DNA damage, p53/TAp63 and AKT regulate mTORC1 through two independent parallel pathways. Conclusion: DNA damage activates Akt, resulting in inhibition of S6K1, whereas Sestrin1/2 downstream of p53 and REDD1 downstream of p63 coordinate to suppress 4E-BP1. Significance: mTORC1-dependent 4EBP1 inhibition by DNA damage is abrogated in most human cancers.",

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AU - Houghton, Peter J.

AU - Cam, Hakan

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AB - Background: mTORC1 integrates cellular inputs and is often deregulated in cancer. Results: In response to DNA damage, p53/TAp63 and AKT regulate mTORC1 through two independent parallel pathways. Conclusion: DNA damage activates Akt, resulting in inhibition of S6K1, whereas Sestrin1/2 downstream of p53 and REDD1 downstream of p63 coordinate to suppress 4E-BP1. Significance: mTORC1-dependent 4EBP1 inhibition by DNA damage is abrogated in most human cancers.

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