@article{LueningschroerSlottaHeimannetal.2020,
  author    = {L{\"u}ningschr{\"o}r, Patrick and Slotta, Carsten and Heimann, Peter and Briese, Michael and Weikert, Ulrich M. and Massih, Bita and Appenzeller, Silke and Sendtner, Michael and Kaltschmidt, Christian and Kaltschmidt, Barbara},
  title     = {Absence of Plekhg5 Results in Myelin Infoldings Corresponding to an Impaired Schwann Cell Autophagy, and a Reduced T-Cell Infiltration Into Peripheral Nerves},
  series = {Frontiers in Cellular Neuroscience},
  volume    = {14},
  journal   = {Frontiers in Cellular Neuroscience},
  issn      = {1662-5102},
  doi       = {10.3389/fncel.2020.00185},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-207538},
  year      = {2020},
  abstract  = {Inflammation and dysregulation of the immune system are hallmarks of several neurodegenerative diseases. An activated immune response is considered to be the cause of myelin breakdown in demyelinating disorders. In the peripheral nervous system (PNS), myelin can be degraded in an autophagy-dependent manner directly by Schwann cells or by macrophages, which are modulated by T-lymphocytes. Here, we show that the NF-κB activator Pleckstrin homology containing family member 5 (Plekhg5) is involved in the regulation of both Schwann cell autophagy and recruitment of T-lymphocytes in peripheral nerves during motoneuron disease. Plekhg5-deficient mice show defective axon/Schwann cell units characterized by myelin infoldings in peripheral nerves. Even at late stages, Plekhg5-deficient mice do not show any signs of demyelination and inflammation. Using RNAseq, we identified a transcriptional signature for an impaired immune response in sciatic nerves, which manifested in a reduced number of CD4\(^+\) and CD8\(^+\) T-cells. These findings identify Plekhg5 as a promising target to impede myelin breakdown in demyelinating PNS disorders.},
  language  = {en}
}
@article{ThangarajSelvarajFrankBenderetal.2012,
  author    = {Thangaraj Selvaraj, Bhuvaneish and Frank, Nicolas and Bender, Florian L. P. and Asan, Esther and Sendtner, Michael},
  title     = {Local axonal function of STAT3 rescues axon degeneration in the pmn model of motoneuron disease},
  series = {The Journal of Cell Biology},
  volume    = {199},
  journal   = {The Journal of Cell Biology},
  number    = {3},
  doi       = {10.1083/jcb.201203109},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-154675},
  pages     = {437 -- 451},
  year      = {2012},
  abstract  = {Axonal maintenance, plasticity, and regeneration are influenced by signals from neighboring cells, in particular Schwann cells of the peripheral nervous system. Schwann cells produce neurotrophic factors, but the mechanisms by which ciliary neurotrophic factor (CNTF) and other neurotrophic molecules modify the axonal cytoskeleton are not well understood. In this paper, we show that activated signal transducer and activator of transcription-3 (STAT3), an intracellular mediator of the effects of CNTF and other neurotrophic cytokines, acts locally in axons of motoneurons to modify the tubulin cytoskeleton. Specifically, we show that activated STAT3 interacted with stathmin and inhibited its microtubule-destabilizing activity. Thus, ectopic CNTF-mediated activation of STAT3 restored axon elongation and maintenance in motoneurons from progressive motor neuronopathy mutant mice, a mouse model of motoneuron disease. This mechanism could also be relevant for other neurodegenerative diseases and provide a target for new therapies for axonal degeneration.},
  language  = {en}
}