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10.1038/nn.3809 http://scihub22266oqcxt.onion/10.1038/nn.3809 C4494117!4494117!25195104     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Neurosci 2014 ; 17 (10): 1351-61 Nephropedia Template TP {{tp|p=25195104|t=2014. Metabolic regulator LKB1 plays a crucial role in Schwann cell-mediated axon maintenance |pdf=|usr=}}{{25195104}} gab.com Text Metabolic regulator LKB1 plays a crucial role in Schwann cell-mediated axon maintenance JO: Nat Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=25195104 #FOAvip Schwann cells (SCs) promote axonal integrity independently of myelination by poorly understood mechanisms. Current models suggest that SC metabolism is critical for this support function and that SC metabolic deficits may lead to axonal demise. The LKB1-AMPK kinase pathway targets multiple downstream effectors including mTOR and is a key metabolic regulator implicated in metabolic diseases. We show through integrative molecular, structural, and behavioral characterization of SC-specific mutant mice that LKB1 activity is central to axon stability, whereas AMPK and mTOR in SCs are largely dispensable. The degeneration of axons in LKB1-mutants is most dramatic in unmyelinated small sensory fibers, whereas motor axons are relatively spared. LKB1 deletion in SCs leads to abnormalities in nerve energy and lipid homeostasis, and increased lactate release. The latter acts in a compensatory manner to support distressed axons. LKB1 signaling is essential for SC-mediated axon support, a function that may be dysregulated in diabetic neuropathy. Twit Text FOAVip Metabolic regulator LKB1 plays a crucial role in Schwann cell-mediated axon maintenance ????Nat Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=25195104 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25195104 #FOAvip English Wikipedia <ref>{{Cite pmid|25195104}}</ref> Metabolic regulator LKB1 plays a crucial role in Schwann cell-mediated axon maintenance #MMPMID25195104 Beirowski B; Babetto E; Golden JP; Chen YJ; Yang K; Gross RW; Patti GJ; Milbrandt J Nat Neurosci 2014[Oct]; 17 (10): 1351-61 PMID25195104show ga Schwann cells (SCs) promote axonal integrity independently of myelination by poorly understood mechanisms. Current models suggest that SC metabolism is critical for this support function and that SC metabolic deficits may lead to axonal demise. The LKB1-AMPK kinase pathway targets multiple downstream effectors including mTOR and is a key metabolic regulator implicated in metabolic diseases. We show through integrative molecular, structural, and behavioral characterization of SC-specific mutant mice that LKB1 activity is central to axon stability, whereas AMPK and mTOR in SCs are largely dispensable. The degeneration of axons in LKB1-mutants is most dramatic in unmyelinated small sensory fibers, whereas motor axons are relatively spared. LKB1 deletion in SCs leads to abnormalities in nerve energy and lipid homeostasis, and increased lactate release. The latter acts in a compensatory manner to support distressed axons. LKB1 signaling is essential for SC-mediated axon support, a function that may be dysregulated in diabetic neuropathy. äMetabolic regulator LKB1 plays a crucial role in Schwann cell-mediated(epmc).pdf DeepDyve Pubget Overpricing