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• W2038176278 abstract "Neuronal 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." @default.
• W2038176278 created "2016-06-24" @default.
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• W2038176278 creator A5041305380 @default.
• W2038176278 date "2008-09-15" @default.
• W2038176278 modified "2023-09-24" @default.
• W2038176278 title "The Tsc1–Tsc2 complex influences neuronal polarity by modulating TORC1 activity and SAD levels: Figure 1." @default.
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• W2038176278 doi "https://doi.org/10.1101/gad.1724108" @default.
• W2038176278 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2749676" @default.
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