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Mammalian target of rapamycin (mTOR) acts as a key sensor of growth factor activation, nutrient availability and energy status, and the inhibition of this protein induces autophagy.
Autophagy is induced via the suppression of mTOR (mean PONDR FIT score of 0.089), a sensor of growth factors and nutrient availability, leading to the release of its inhibitory effects on the ULK1 kinase complex (mean PONDR FIT score of 0.546).
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The presence of amino acids stimulates the recruitment of mTORC1 to the late endosomal and lysosomal compartments, which enables mTORC1 to interact with sensors of growth factor signaling (Zoncu et al., 2011).
mTORC1 is a key sensor of nutrients, growth factors, and stress and controls cell metabolism, growth, and survival.
mTOR functions as a sensor of mitogens, growth factors and energy and nutrient levels, facilitating cell-cycle progression from G1-S phase in appropriate growth conditions.
The mammalian target of rapamycin (mTOR), an important sensor of insulin, growth factor, and mitogen inputs, has been revealed in circadian control through many effector proteins.
The mTOR pathway is a sensor of nutrients, growth factors, hormones, mitogens, and cytokines.
The mammalian TOR (mTOR) is encoded by FRAP1 and acts as a sensor of energy, nutrients, growth factors, redox and stress to increase protein synthesis and inhibit autophagy.
mTORC1 is also a sensor of various signals including growth factors, insulin, nutrients, energy status, and cellular stressors.
178, 184 While mechanisms by which JNK participates in the recovery of mitochondrial oxidative metabolism are incompletely defined, one role that JNK plays in the repair of damaged DNA is controlling the expression of the stress sensor protein growth arrest and DNA damage (GADD) 45α.
Other research has suggested that mTOR [mammalian target of rapamycin], an important intracellular energy sensor and growth regulator, also helps regulate pubertal timing and reproductive function [ 63].
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