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Upstream Regulation of micronutrients on mTORC1 - Coggle Diagram
Upstream Regulation of micronutrients on mTORC1
Vitamins
Vitamin D
Suppresses mTORC1 signalling activity through both genomic and non-genomic pathways.
Vitamin C
Suppresses mTORC1 at pharmacological levels through ROS production.
Minerals
Copper
Influences (typically up-regulating) mTORC1 through mitochondrial signalling and compensatory nutrient sensing.
Iron
Iron acts as an upstream regulator by controlling amino acid transporter expression. Demethylates H3K9me2 at LAT3 and RPTOR enhancer regions, increasing their expression (upregulating mTORC1 activity).
Zinc
Promotes mTORC1 activation through direct stimulation of kinases and growth factor signalling enhancement.
Magnesium
Acts as a cofactor (ATP-Mg²⁺), enabling mTORC1 enzymatic function.
Manganese
Activates mTORC1 via upstream kinase AKT1.
Selenium
Indirectly supports mTORC1 by preventing ROS accumulation, thus sustaining redox-sensitive anabolic signalling.
Calcium
Regulates mTORC1 through lysosomal Ca²⁺ dynamics, at MCOLN1 & NCAPD2
Niacin
Activates mTORC1 through GPR109A, a G-protein-coupled receptor responsive to β-hydroxybutyrate.
Folate
Support mTORC1 signaling by maintaining proper DNA methylation and metabolic cofactor availability.
Alpha-Lipoic Acid
Suppresses mTORC1 activity via inhibition of insulin signaling and activation of AMPK.