{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kim WY"],"funding":["NINDS NIH HHS","National Institutes of Health"],"pagination":["981-96"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4167845"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["52(6)"],"pubmed_abstract":["Glycogen synthase kinase-3beta (GSK-3beta) is thought to mediate morphological responses to a variety of extracellular signals. Surprisingly, we found no gross morphological deficits in nervous system development in GSK-3beta null mice. We therefore designed an shRNA that targeted both GSK-3 isoforms. Strong knockdown of both GSK-3alpha and beta markedly reduced axon growth in dissociated cultures and slice preparations. We then assessed the role of different GSK-3 substrates in regulating axon morphology. Elimination of activity toward primed substrates only using the GSK-3 R96A mutant was associated with a defect in axon polarity (axon branching) compared to an overall reduction in axon growth induced by a kinase-dead mutant. Consistent with this finding, moderate reduction of GSK-3 acti"],"journal":["Neuron"],"pubmed_title":["Essential roles for GSK-3s and GSK-3-primed substrates in neurotrophin-induced and hippocampal axon growth."],"pmcid":["PMC4167845"],"funding_grant_id":["R01 NS050968","R01NS050968"],"pubmed_authors":["Wang YM","Kaibuchi K","Anton ES","Yokota Y","Kim WY","Woodgett JR","Zhou FQ","Snider WD","Zhou J","Yoshimura T"],"additional_accession":[]},"is_claimable":false,"name":"Essential roles for GSK-3s and GSK-3-primed substrates in neurotrophin-induced and hippocampal axon growth.","description":"Glycogen synthase kinase-3beta (GSK-3beta) is thought to mediate morphological responses to a variety of extracellular signals. Surprisingly, we found no gross morphological deficits in nervous system development in GSK-3beta null mice. We therefore designed an shRNA that targeted both GSK-3 isoforms. Strong knockdown of both GSK-3alpha and beta markedly reduced axon growth in dissociated cultures and slice preparations. We then assessed the role of different GSK-3 substrates in regulating axon morphology. Elimination of activity toward primed substrates only using the GSK-3 R96A mutant was associated with a defect in axon polarity (axon branching) compared to an overall reduction in axon growth induced by a kinase-dead mutant. Consistent with this finding, moderate reduction of GSK-3 acti","dates":{"release":"2006-01-01T00:00:00Z","publication":"2006 Dec","modification":"2025-06-28T03:05:22.773Z","creation":"2025-06-28T03:05:22.773Z"},"accession":"S-EPMC4167845","cross_references":{"pubmed":["17178402"],"doi":["10.1016/j.neuron.2006.10.031"]}}