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lüll The Tsc1-Tsc2 complex influences neuronal polarity by modulating TORC1 activity and SAD levels Wildonger J; Jan LY; Jan YNGenes Dev 2008[Sep]; 22 (18): 2447-53Neuronal function depends on the specification of neuronal processes as axons or dendrites. In this issue of Genes & Development Choi and colleagues (2485-2495) show that without Tuberous Sclerosis Complex 1 (Tsc1) or Tsc2, molecules linked to the autosomal dominant disease tuberous sclerosis, an increase in the activity of the translational regulator Target of Rapamycin 1 (TORC1) causes neurons to have multiple axons and the translation of SAD kinase increases as well. Thus, in addition to the kinase LKB1, the Tsc1-Tsc2 complex, acting through TORC1, also modulates SAD to regulate axon formation.|Cell Division/physiology[MESH]|Humans[MESH]|Intracellular Signaling Peptides and Proteins/*metabolism[MESH]|Mechanistic Target of Rapamycin Complex 1[MESH]|Multiprotein Complexes[MESH]|Neurons/*physiology[MESH]|Protein Serine-Threonine Kinases/*metabolism[MESH]|Proteins[MESH]|TOR Serine-Threonine Kinases[MESH]|Transcription Factors/*metabolism[MESH]|Tuberous Sclerosis Complex 1 Protein[MESH]|Tuberous Sclerosis Complex 2 Protein[MESH]|Tumor Suppressor Proteins/metabolism/*physiology[MESH] |