The upstream regulators of TFEB and its downstream signaling pathways. For example, mTORC1 is attracted to the lysosomal membrane under nutrient-rich circumstances, such as amino stimulation. The lysosomal membrane allows amino acids to readily pass and accumulate inside the lysosomes. This signals the TFEB’s deactivation. However, when nutrients are few, TFEB becomes unphosphorylated and active. The expression of target genes, including as those involved in ALB, is subsequently increased as a result of active TFEB’s subsequent nuclear translocation, CLEAR motif binding, and activation of gene expression.
Akt, AKT serine/threonine kinase; ALB, autophagy–lysosomal biogenesis; CLEAR, coordinating lysosomal expression and regulation; ERK, extracellular signal-regulated kinase; LAG, lysosomal–autophagic genes; mTORC1, mammalian target of rapamycin complex 1; PAR, poly ADP-ribosyl; PGC1α, peroxisome proliferator-activated receptor gamma coactivator-1 alpha; PKC, PKC, protein kinase; PPAR-α, peroxisome proliferator-activated receptor alpha; RANKL, receptor activator of nuclear factor-κB ligand; TCF/LEF, T-cell factor/lymphoid enhancer factor; TSC, tuberous sclerosis complex; p, phosphate; TFEB, transcription factor EB.