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 | |
| State | Published - Feb 14 2014 |
| Externally published | Yes |
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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 journal › Article
}
TY - JOUR
T1 - P53/TAp63 and AKT regulate mammalian target of rapamycin complex 1 (mTORC1) signaling through two independent parallel pathways in the presence of DNA damage
AU - Cam, Maren
AU - Bid, Hemant K.
AU - Xiao, Linlin
AU - Zambetti, Gerard P.
AU - Houghton, Peter J
AU - Cam, Hakan
PY - 2014/2/14
Y1 - 2014/2/14
N2 - 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.
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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UR - http://www.scopus.com/inward/citedby.url?scp=84894122839&partnerID=8YFLogxK
U2 - 10.1074/jbc.M113.530303
DO - 10.1074/jbc.M113.530303
M3 - Article
C2 - 24366874
AN - SCOPUS:84894122839
VL - 289
SP - 4083
EP - 4094
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
SN - 0021-9258
IS - 7
ER -