PMID- 19200882
OWN - NLM
STAT- MEDLINE
DCOM- 20090402
LR  - 20211203
IS  - 1557-7988 (Electronic)
IS  - 0076-6879 (Linking)
VI  - 452
DP  - 2009
TI  - Monitoring mammalian target of rapamycin (mTOR) activity.
PG  - 165-80
LID - 10.1016/S0076-6879(08)03611-2 [doi]
AB  - Mammalian target of rapamycin (mTOR) is an evolutionarily conserved 
      serine/threonine protein kinase implicated in a wide array of cellular processes 
      such as cell growth, proliferation, and survival. Analogous to the situation in 
      yeast, mTOR forms two distinct functional complexes termed mTOR complex 1 and 2 
      (mTORC1 and mTORC2). mTORC1 activity is inhibited by rapamycin, a specific 
      inhibitor of mTOR, whereas mTORC2 activity is resistant to short-term treatments 
      with rapamycin. In response to growth factors, mTORC2 phosphorylates Akt, an 
      essential kinase involved in cell survival. On the other hand, mTORC1 can be 
      activated by both growth factors and nutrients such as glucose and amino acids. 
      In turn, mTORC1 regulates the activity of the translational machinery by 
      modulating S6 kinase (S6K) activity and eIF4E binding protein 1 (4E-BP1) through 
      direct phosphorylation. Consequently, protein synthesis and cell growth are 
      stimulated in a variety of different cell types. In addition, mTORC1 inhibits 
      autophagy, an essential protein degradation and recycling system, which cells 
      employ to sustain their viability in times of limited availability of nutrients. 
      Recent studies have highlighted the fact that autophagy plays crucial roles in 
      many aspects of human health including cancer development, neurodegenerative 
      disease, diabetes, and aging. It is likely that dysregulation of the 
      mTOR-autophagy pathway may contribute at least in part to these human disorders. 
      Therefore, the assessment of mTOR activity is important to understand the status 
      of autophagy in the cells being analyzed and its role in autophagy-related 
      disorders. In this section, we describe methods to monitor mTOR activity both in 
      vitro and in vivo.
FAU - Ikenoue, Tsuneo
AU  - Ikenoue T
AD  - Life Sciences Institute, University of Michigan, Ann Arbor, Michigan, USA.
FAU - Hong, Sungki
AU  - Hong S
FAU - Inoki, Ken
AU  - Inoki K
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Methods Enzymol
JT  - Methods in enzymology
JID - 0212271
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Autophagy/physiology
MH  - Cell Line
MH  - Humans
MH  - Immunohistochemistry
MH  - In Vitro Techniques
MH  - Protein Kinases/*metabolism
MH  - TOR Serine-Threonine Kinases
EDAT- 2009/02/10 09:00
MHDA- 2009/04/03 09:00
CRDT- 2009/02/10 09:00
PHST- 2009/02/10 09:00 [entrez]
PHST- 2009/02/10 09:00 [pubmed]
PHST- 2009/04/03 09:00 [medline]
AID - S0076-6879(08)03611-2 [pii]
AID - 10.1016/S0076-6879(08)03611-2 [doi]
PST - ppublish
SO  - Methods Enzymol. 2009;452:165-80. doi: 10.1016/S0076-6879(08)03611-2.