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024 7 _ |a 10.1016/j.neuron.2016.09.026
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024 7 _ |a 0896-6273
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024 7 _ |a 1097-4199
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037 _ _ |a DZNE-2020-05179
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Tedeschi, Andrea
|0 P:(DE-2719)2810470
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|e First author
245 _ _ |a The Calcium Channel Subunit Alpha2delta2 Suppresses Axon Regeneration in the Adult CNS.
260 _ _ |a New York, NY
|c 2016
|b Elsevier
264 _ 1 |3 print
|2 Crossref
|b Elsevier BV
|c 2016-10-01
336 7 _ |a article
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336 7 _ |a ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a Injuries to the adult CNS often result in permanent disabilities because neurons lose the ability to regenerate their axon during development. Here, whole transcriptome sequencing and bioinformatics analysis followed by gain- and loss-of-function experiments identified Cacna2d2, the gene encoding the Alpha2delta2 subunit of voltage-gated calcium channels (VGCCs), as a developmental switch that limits axon growth and regeneration. Cacna2d2 gene deletion or silencing promoted axon growth in vitro. In vivo, Alpha2delta2 pharmacological blockade through Pregabalin (PGB) administration enhanced axon regeneration in adult mice after spinal cord injury (SCI). As PGB is already an established treatment for a wide range of neurological disorders, our findings suggest that targeting Alpha2delta2 may be a novel treatment strategy to promote structural plasticity and regeneration following CNS trauma.
536 _ _ |a 341 - Molecular Signaling (POF3-341)
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542 _ _ |i 2016-10-01
|2 Crossref
|u https://www.elsevier.com/tdm/userlicense/1.0/
542 _ _ |i 2017-10-19
|2 Crossref
|u https://www.elsevier.com/open-access/userlicense/1.0/
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Cacna2d2 protein, mouse
|2 NLM Chemicals
650 _ 7 |a Calcium Channel Blockers
|2 NLM Chemicals
650 _ 7 |a Calcium Channels
|2 NLM Chemicals
650 _ 7 |a RNA, Messenger
|2 NLM Chemicals
650 _ 7 |a Pregabalin
|0 55JG375S6M
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Axons: drug effects
|2 MeSH
650 _ 2 |a Axons: physiology
|2 MeSH
650 _ 2 |a Calcium Channel Blockers: pharmacology
|2 MeSH
650 _ 2 |a Calcium Channels: drug effects
|2 MeSH
650 _ 2 |a Calcium Channels: genetics
|2 MeSH
650 _ 2 |a Calcium Channels: metabolism
|2 MeSH
650 _ 2 |a Central Nervous System
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Ganglia, Spinal: cytology
|2 MeSH
650 _ 2 |a Ganglia, Spinal: metabolism
|2 MeSH
650 _ 2 |a Gene Expression Profiling
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Mice, Knockout
|2 MeSH
650 _ 2 |a Neuronal Outgrowth: drug effects
|2 MeSH
650 _ 2 |a Neuronal Outgrowth: genetics
|2 MeSH
650 _ 2 |a Neurons: metabolism
|2 MeSH
650 _ 2 |a Pregabalin: pharmacology
|2 MeSH
650 _ 2 |a RNA, Messenger: metabolism
|2 MeSH
650 _ 2 |a Regeneration: drug effects
|2 MeSH
650 _ 2 |a Regeneration: genetics
|2 MeSH
650 _ 2 |a Sequence Analysis, RNA
|2 MeSH
650 _ 2 |a Spinal Cord Injuries: metabolism
|2 MeSH
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|e Platform for Single Cell Genomics and Epigenomics at DZNE University of Bonn
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700 1 _ |a Dupraz, Sebastian
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700 1 _ |a Laskowski, Claudia J
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700 1 _ |a Xue, Jia
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700 1 _ |a Ulas, Thomas
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700 1 _ |a Beyer, Marc
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700 1 _ |a Schultze, Joachim L
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700 1 _ |a Bradke, Frank
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773 1 8 |a 10.1016/j.neuron.2016.09.026
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773 _ _ |a 10.1016/j.neuron.2016.09.026
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Marc 21