ArticleCommunicative & integrative biology2018
Multiple lines of inhibitory feedback on AKT kinase in Schwann cells lacking TSC1/2 hint at distinct functions of mTORC1 and AKT in nerve development.
Article in Communicative & integrative biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Growth factors-based therapeutic strategies and their underlying signaling mechanisms for peripheral nerve regeneration.Acta pharmacologica Sinica · 2020Review
- Adult tissue-derived neural crest-like stem cells: Sources, regulatory networks, and translational potential.Stem cells translational medicine · 2020Review
- [Changes in expression of microRNA-221 and phosphatase and tension protein homologue in nerve stump after peripheral nerve injury].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2019Article
- Myelinating Schwann cells ensheath multiple axons in the absence of E3 ligase component Fbxw7.Nature communications · 2019Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During nerve development, Schwann cells (SCs) build multilayered myelin sheaths around axons to accelerate nerve conduction. The mechanistic target of rapamycin complex 1 (mTORC1) downstream of PI3K/AKT signaling lately emerged as a central anabolic regulator of myelination. Using mutant mice with sustained mTORC1 hyperactivity in developing SCs we recently uncovered that mTORC1 impedes developmental myelination by promoting proliferation of immature SCs while antagonizing SC differentiation. In contrast, mTORC1 stimulates myelin production, rather than SC proliferation, in already differentiated SCs. Importantly, these diametrical mTORC1 functions were unmasked under settings of greatly suppressed AKT signaling. Here we demonstrate, inter alia, additional mechanisms of feedback inhibition of AKT by mTORC1, such as strikingly elevated PTEN levels in SCs with disruption of the mTORC1 inhibitory complex, TSC1/2. These data lead us to propose a model wherein mTORC1 and AKT have distinct roles in developing SCs that have to be precisely coordinated for normal myelinogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.