PMID- 21871173
OWN - NLM
STAT- MEDLINE
DCOM- 20111227
LR  - 20211203
IS  - 1976-670X (Electronic)
IS  - 1976-6696 (Linking)
VI  - 44
IP  - 8
DP  - 2011 Aug
TI  - The functions of mTOR in ischemic diseases.
PG  - 506-11
AB  - Mammalian Target of Rapamycin (mTOR) is a serine/threonine kinase and that forms 
      two multiprotein complexes known as the mTOR complex 1 (mTORC1) and mTOR complex 
      2 (mTORC2). mTOR regulates cell growth, proliferation and survival. mTORC1 is 
      composed of the mTOR catalytic subunit and three associated proteins: raptor, 
      mLST8/GbetaL and PRAS40. mTORC2 contains mTOR, rictor, mLST8/GbetaL, mSin1, and protor. 
      Here, we discuss mTOR as a promising anti-ischemic agent. It is believed that 
      mTORC2 lies down-stream of Akt and acts as a direct activator of Akt. The 
      different functions of mTOR can be explained by the existence of two distinct 
      mTOR complexes containing unique interacting proteins. The loss of TSC2, which is 
      upstream of mTOR, activates S6K1, promotes cell growth and survival, activates 
      mTOR kinase activities, inhibits mTORC1 and mTORC2 via mTOR inhibitors, and 
      suppresses S6K1 and Akt. Although mTOR signaling pathways are often activated in 
      human diseases, such as cancer, mTOR signaling pathways are deactivated in 
      ischemic diseases. From Drosophila to humans, mTOR is necessary for Ser473 
      phosphorylation of Akt, and the regulation of Akt-mTOR signaling pathways may 
      have a potential role in ischemic disease. This review evaluates the potential 
      functions of mTOR in ischemic diseases. A novel mTOR-interacting protein 
      deregulates over-expression in ischemic disease, representing a new mechanism for 
      controlling mTOR signaling pathways and potential therapeutic strategies for 
      ischemic diseases.
FAU - Hwang, Seo-Kyoung
AU  - Hwang SK
AD  - Vascular Medicine Research Unit, Department of Medicine, Brigham and Women's 
      Hospital, Harvard Medical School, Boston, Massachusetts, USA.
FAU - Kim, Hyung-Hwan
AU  - Kim HH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Korea (South)
TA  - BMB Rep
JT  - BMB reports
JID - 101465334
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Humans
MH  - Ischemia/*enzymology/*pathology
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/*metabolism
EDAT- 2011/08/30 06:00
MHDA- 2011/12/28 06:00
CRDT- 2011/08/30 06:00
PHST- 2011/08/30 06:00 [entrez]
PHST- 2011/08/30 06:00 [pubmed]
PHST- 2011/12/28 06:00 [medline]
AID - 10.5483/bmbrep.2011.44.8.506 [doi]
PST - ppublish
SO  - BMB Rep. 2011 Aug;44(8):506-11. doi: 10.5483/bmbrep.2011.44.8.506.