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10.1080/19336918.2016.1210758

http://scihub22266oqcxt.onion/10.1080/19336918.2016.1210758
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C5160031!5160031!27392015
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suck abstract from ncbi


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pmid27392015      Cell+Adh+Migr 2016 ; 10 (6): 627-40
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  • Regulation of dendritic development by semaphorin 3A through novel intracellular remote signaling #MMPMID27392015
  • Goshima Y; Yamashita N; Nakamura F; Sasaki Y
  • Cell Adh Migr 2016[]; 10 (6): 627-40 PMID27392015show ga
  • Numerous cell adhesion molecules, extracellular matrix proteins and axon guidance molecules participate in neuronal network formation through local effects at axo-dendritic, axo-axonic or dendro-dendritic contact sites. In contrast, neurotrophins and their receptors play crucial roles in neural wiring by sending retrograde signals to remote cell bodies. Semaphorin 3A (Sema3A), a prototype of secreted type 3 semaphorins, is implicated in axon repulsion, dendritic branching and synapse formation via binding protein neuropilin-1 (NRP1) and the signal transducing protein PlexinAs (PlexAs) complex. This review focuses on Sema3A retrograde signaling that regulates dendritic localization of AMPA-type glutamate receptor GluA2 and dendritic patterning. This signaling is elicited by activation of NRP1 in growth cones and is propagated to cell bodies by dynein-dependent retrograde axonal transport of PlexAs. It also requires interaction between PlexAs and a high-affinity receptor for nerve growth factor, toropomyosin receptor kinase A. We propose a control mechanism by which retrograde Sema3A signaling regulates the glutamate receptor localization through trafficking of cis-interacting PlexAs with GluA2 along dendrites; this remote signaling may be an alternative mechanism to local adhesive contacts for neural network formation.
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