Journal
GENES & DEVELOPMENT
Volume 22, Issue 18, Pages 2447-2453Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1724108
Keywords
neuronal polarity; tuberous sclerosis complex; TSC; SAD; kinase; autism
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Funding
- Howard Hughes Medical Institute Funding Source: Medline
- NICHD NIH HHS [F32 HD053199, F32 HD053199-02, F32 HD053199-01A1] Funding Source: Medline
- NIMH NIH HHS [R01 MH084234] Funding Source: Medline
- NINDS NIH HHS [R01 NS047200, R01 NS047200-04, R01 NS040929-07, R37 NS040929, R01 NS040929-08, R01 NS047200-03, R01 NS040929] Funding Source: Medline
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Neuronal function depends on the specification of neuronal processes as axons or dendrites. In this issue of Genes & Development Choi and colleagues ( pp. 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.
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