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 journalArticle

34 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)4083-4094
Number of pages12
JournalJournal of Biological Chemistry
Volume289
Issue number7
DOIs
StatePublished - Feb 14 2014
Externally publishedYes

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DNA Damage
DNA
Neoplasms
mechanistic target of rapamycin complex 1

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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 journalArticle

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