mTORMammalian Target of Rapamycin (a protein)
mTORMan, Technology, Organisation and Risk Management
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This increase in cAMP is what then interferes with the master switch mTOR, shutting it down.
However, they never tested tumour tissue from those patients to understand the molecular role of mTOR.
Bringing these streams together, we hypothesise that calcium dependent NFAT activation downstream of TAK1 and mTOR isa critical pathway for myofibroblast differentiation and pro-fibrotic gene expression.
Excess mTOR can stimulate cell growth and block autophagy, which is removal of accumulated waste products inside cells.
Why, exactly, does mTOR activity slow down in an acidic environment?
Mammalian target of rapamycin (mTOR) is a master sensor of energy status and will be inhibited in the state of energy depletion.[15] Myocardial energy depletion plays a major role in myocardial dysfunction during sepsis.[16],[17] There are little data describing the role of the mTOR pathway during sepsis in the heart.[18] Furthermore, among various pathways known to regulate autophagy in mammalian cells, mTOR complex 1 (mTORC1)/S6 kinase-1 (S6K1) signaling pathway is one of the best-understood pathways.[19] Accumulating evidence has indicated that the mTORC1/S6K1 pathway negatively regulates autophagy, so the relationship between the mTOR pathway and the change of autophagy process in cecal ligation and puncture (CLP)-induced myocardial dysfunction was investigated in this study.
The enzyme mammalian (or mechanistic) target of rapamycin (mTOR) plays a key role in the control of crucial cell processes; it regulates growth and keeps it in a state of equilibrium.
The upgrade of MTOR's ratings is driven by the significant improvement in the company's credit profile over the past year.
Oral NaB group showed decreased genetic expression of AMPK (0.04 fold, p<0.001), mTOR (0.30 fold, p=0.04), Akt (0.29 fold, p=0.67) and Sirt1 (0.83 fold, p=0.18).
Following its direct phosphorylation by ULK-1, in response to inhibition by mTOR in mammals, Beclin-1 activates hVPS34.
Recently it has been reported that in young animals the intracellular signalling mechanism, the mammalian target of rapamycin (mTOR), is activated by the rise of plasma insulin and amino acids concentration, which in turn increases the rate of protein synthesis [7-9].
The antiepileptic medication vigabatrin is particularly effective in treating infantile spasms in TSC and has mTOR [mechanistic target of the rapamycin]-inhibiting effects.