PMID- 22680924
OWN - NLM
STAT- MEDLINE
DCOM- 20121212
LR  - 20220408
IS  - 1875-533X (Electronic)
IS  - 0929-8673 (Print)
IS  - 0929-8673 (Linking)
VI  - 19
IP  - 22
DP  - 2012
TI  - Homeostasis and the importance for a balance between AKT/mTOR activity and 
      intracellular signaling.
PG  - 3748-62
AB  - The AKT family of serine threonine kinases is of critical importance with regard 
      to growth factor signaling, cell proliferation, survival and oncogenesis. 
      Engagement of signaling receptors induces the lipid kinase, phosphatidylinositol 
      3-kinase (PI3K), which enables the activation of AKT. Responsive to the PI3K/AKT 
      pathway is the mammalian target of rapamycin (mTOR), a major effector that is 
      specifically implicated in the regulation of cell growth as a result of nutrient 
      availability and cellular bioenergetics. These kinases mediate the activity of a 
      multitude of intracellular signaling molecules and intersect with multiple 
      pathways that regulate cellular processes. Elucidating the role of AKT/mTOR in 
      metabolism and in hallmark signaling pathways that are aberrantly affected in 
      cancer has provided a solid foundation of discoveries. From this, new research 
      directions are emerging with regard to the role of AKT/mTOR in diabetes and T 
      cell-mediated immunity. As a result, a new perspective is developing in how 
      AKT/mTOR functions within intracellular signaling pathways to maintain cellular 
      homeostasis. An appreciation is emerging that altered equilibrium of AKT/mTOR 
      pathways contributes to disease and malignancy. Such new insights may lead to 
      novel intervention strategies that may be useful to reprogram or reset the 
      balance of intracellular signaling.
FAU - Altomare, D A
AU  - Altomare DA
AD  - Burnett School of Biomedical Sciences, College of Medicine, University of Central 
      Florida, 6900 Lake Nona Blvd., Orlando, FL 32827, USA. deborah.altomare@ucf.edu
FAU - Khaled, A R
AU  - Khaled AR
LA  - eng
GR  - R21 CA129302/CA/NCI NIH HHS/United States
GR  - CA129302/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United Arab Emirates
TA  - Curr Med Chem
JT  - Current medicinal chemistry
JID - 9440157
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Protein Isoforms)
RN  - 0 (Protein Kinase Inhibitors)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Homeostasis/drug effects
MH  - Humans
MH  - Intercellular Signaling Peptides and Proteins/metabolism
MH  - Lymphocytes/immunology/metabolism
MH  - Neoplasms/drug therapy/metabolism/pathology
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Protein Isoforms/metabolism
MH  - Protein Kinase Inhibitors/pharmacology/therapeutic use
MH  - Proto-Oncogene Proteins c-akt/antagonists & inhibitors/*metabolism
MH  - Signal Transduction/*drug effects
MH  - TOR Serine-Threonine Kinases/antagonists & inhibitors/*metabolism
PMC - PMC3414727
EDAT- 2012/06/12 06:00
MHDA- 2012/12/13 06:00
PMCR- 2012/08/09
CRDT- 2012/06/12 06:00
PHST- 2012/12/14 00:00 [received]
PHST- 2012/04/03 00:00 [revised]
PHST- 2012/04/16 00:00 [accepted]
PHST- 2012/06/12 06:00 [entrez]
PHST- 2012/06/12 06:00 [pubmed]
PHST- 2012/12/13 06:00 [medline]
PHST- 2012/08/09 00:00 [pmc-release]
AID - CMC-EPUB-20120607-24 [pii]
AID - CMC-19-3748 [pii]
AID - 10.2174/092986712801661130 [doi]
PST - ppublish
SO  - Curr Med Chem. 2012;19(22):3748-62. doi: 10.2174/092986712801661130.