期刊
CANCER RESEARCH
卷 67, 期 1, 页码 1-4出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-06-3016
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资金
- NATIONAL CANCER INSTITUTE [R01CA046677, R29CA046677] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [S06GM060654] Funding Source: NIH RePORTER
- NCI NIH HHS [CA 46677] Funding Source: Medline
- NCRR NIH HHS [RR 03037] Funding Source: Medline
- NIGMS NIH HHS [GM 60654] Funding Source: Medline
Interest in the regulation of the mammalian target of rapamycin (mTOR) has increased substantially in recent years largely because of an apparent link between mTOR and survival signals in human cancer cells. Much has been learned about the regulation of mTOR in response to survival signals generated by phosphatidylinositol 3-kinase (PI3K). However, another mechanism for regulating mTOR has been proposed involving the generation of phosphatidic acid (PA). PA is the metabolic product of phospholipase D (PLD), whose activity is elevated in a large number of human cancers, and, like PI3K, has been implicated in the survival of human cancer cells. Although the regulation of mTOR by the PI3K signaling pathway is well established, a role for PLD and PA in regulating mTOR has been controversial. In this review, the evidence implicating PLD and PA in the regulation of mTOR is summarized, and the implications of this novel and potentially important mechanism for regulating mTOR are discussed.
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