TFEB, the transcription factor EB, is a master regulator in the autophagy/lysosomal-to-nucleus signaling pathway, belonging to the MiT/TFE family of basic helix-loop-helix leucine zipper transcription factors [4]. It plays a pivotal role in regulating basic cellular processes such as lysosomal biogenesis and autophagy. TFEB's activity is closely associated with multiple signaling pathways, including mTOR, Wnt, calcium, and AKT, and is crucial for energy homeostasis, stress response, and metabolism [4].

In vivo studies, potentially including KO/CKO mouse models though not explicitly detailed in the provided abstracts, have shown that TFEB is involved in lipid catabolism [1]. Also, TFEB has been found to be capable of inducing the intracellular clearance of pathogenic factors in murine models of diseases like Parkinson's and Alzheimer's, suggesting its potential in developing novel therapeutic strategies [1]. In autophagy, TFEB coordinates a transcriptional program controlling autophagosome formation, autophagosome-lysosome fusion, and substrate degradation during starvation, by driving the expression of autophagy and lysosomal genes [2]. The ubiquitin-proteasome pathway, through the E3 ubiquitin ligase STUB1, modulates TFEB activity, affecting autophagy and mitochondrial biogenesis [3].

In conclusion, TFEB is a central regulator of lysosomal biogenesis, autophagy, and other cellular processes. Model-based research, potentially including KO/CKO mouse models, has revealed its significance in neurodegenerative diseases, lipid catabolism, and autophagy-related functions. Understanding TFEB's role provides insights into disease mechanisms and potential therapeutic targets for neurodegenerative and other related diseases.