Summary
The function of the mammalian target of rapamycin (mTOR) is upregulated 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 mTORI 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, endoplasmic 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.
Keywords
MEG-01 cells - raptor - rictor - mTOR - rapamycin - torin1 - apoptosis - calcium homeostasis