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Role of mTOR1 and mTOR2 complexes in MEG-01 cell physiology
被引:6
作者:
Lopez, Esther
[1
]
Berna-Erro, Alejandro
[1
]
Lopez, Javier J.
[1
]
Granados, Maria P.
[1
]
Bermejo, Nuria
[2
]
Brull, Jose M.
[3
]
Salido, Gines M.
[1
]
Rosado, Juan A.
[1
]
Redondo, Pedro C.
[1
]
机构:
[1] Univ Extremadura, Dept Physiol PHYCELL, Caceres, Spain
[2] San Pedro de Alcantara Hosp, Hematol Unit, Caceres, Spain
[3] Blood Donat Ctr Extremadura, Merida, Spain
关键词:
MEG-01;
cells;
raptor;
rictor;
mTOR;
rapamycin;
torin1;
apoptosis;
calcium homeostasis;
THROMBOPOIETIN RECEPTOR AGONIST;
ENDOPLASMIC-RETICULUM;
MAMMALIAN TARGET;
TRANSPLANT PATIENTS;
CANCER-CELLS;
RAPAMYCIN;
APOPTOSIS;
MITOCHONDRIA;
FKBP38;
DIFFERENTIATION;
D O I:
10.1160/TH14-09-0727
中图分类号:
R5 [内科学];
学科分类号:
1002 ;
100201 ;
摘要:
The function of the mammalian target of rapamycin (mTOR) is up-regulated in response to cell stimulation with growing and differentiating factors. Active mTOR controls cell proliferation, differentiation and death. Since mTOR associates with different proteins to form two functional macromolecular complexes, we aimed to investigate the role of the mTOR1 and mTOR2 complexes in MEG-01 cell physiology in response to thrombopoietin (TPO). By using mTOR antagonists and overexpressing FKBP38, we have explored the role of both mTOR complexes in proliferation, apoptosis, maturation-like mechanisms, endo-plasmic reticulum-stress and the intracellular location of both active mTOR complexes during MEG-01 cell stimulation with TPO. The results demonstrate that mTOR1 and mTOR2 complexes play different roles in the physiology of MEG-01 cells and in the maturation-like mechanisms; hence, these findings might help to understand the mechanism underlying generation of platelets.
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页码:969 / 981
页数:13
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