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000140176 0247_ $$2doi$$a10.1242/jcs.216101
000140176 0247_ $$2pmid$$apmid:29898920
000140176 0247_ $$2ISSN$$a0021-9533
000140176 0247_ $$2ISSN$$a0370-2952
000140176 0247_ $$2ISSN$$a1477-9137
000140176 0247_ $$2altmetric$$aaltmetric:63726834
000140176 037__ $$aDZNE-2020-06498
000140176 041__ $$aEnglish
000140176 082__ $$a570
000140176 1001_ $$aFerrari, María E$$b0
000140176 245__ $$aWnt7b signalling through Frizzled-7 receptor promotes dendrite development by coactivating CaMKII and JNK.
000140176 260__ $$aCambridge$$bCompany of Biologists Limited$$c2018
000140176 264_1 $$2Crossref$$3online$$bThe Company of Biologists$$c2018-06-13
000140176 264_1 $$2Crossref$$3print$$bThe Company of Biologists$$c2018-07-01
000140176 3367_ $$2DRIVER$$aarticle
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000140176 3367_ $$2BibTeX$$aARTICLE
000140176 3367_ $$2ORCID$$aJOURNAL_ARTICLE
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000140176 520__ $$aThe formation of complex dendritic arbors is crucial for the assembly of functional networks as abnormal dendrite formation underlies several neurodevelopmental and psychiatric disorders. Many extracellular factors have been postulated as regulators of dendritic growth. Wnt proteins play a critical role in neuronal development and circuit formation. We previously demonstrated that Wnt7b acts through the scaffold protein dishevelled 1 (Dvl1) to modulate dendrite arborisation by activating a non-canonical Wnt signalling pathway. Here, we identify the seven-transmembrane frizzled-7 (Fz7, also known as FZD7) as the receptor for Wnt7b-mediated dendrite growth and complexity. Importantly, Fz7 is developmentally regulated in the intact hippocampus, and is localised along neurites and at dendritic growth cones, suggesting a role in dendrite formation and maturation. Fz7 loss-of-function studies demonstrated that Wnt7b requires Fz7 to promote dendritic arborisation. Moreover, in vivo Fz7 loss of function results in dendritic defects in the intact mouse hippocampus. Furthermore, our findings reveal that Wnt7b and Fz7 induce the phosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and JNK proteins, which are required for dendritic development. Here, we demonstrate that Wnt7b-Fz7 signals through two non-canonical Wnt pathways to modulate dendritic growth and complexity.
000140176 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
000140176 536__ $$0G:(DE-HGF)POF3-341$$a341 - Molecular Signaling (POF3-341)$$cPOF3-341$$fPOF III$$x1
000140176 542__ $$2Crossref$$i2019-01-01$$uhttp://www.biologists.com/user-licence-1-1/
000140176 588__ $$aDataset connected to CrossRef, PubMed,
000140176 650_7 $$2NLM Chemicals$$aDishevelled Proteins
000140176 650_7 $$2NLM Chemicals$$aDvl1 protein, mouse
000140176 650_7 $$2NLM Chemicals$$aFzd7 protein, mouse
000140176 650_7 $$2NLM Chemicals$$aProto-Oncogene Proteins
000140176 650_7 $$2NLM Chemicals$$aReceptors, G-Protein-Coupled
000140176 650_7 $$2NLM Chemicals$$aWnt Proteins
000140176 650_7 $$2NLM Chemicals$$aWnt7b protein, mouse
000140176 650_7 $$0EC 2.7.11.17$$2NLM Chemicals$$aCalcium-Calmodulin-Dependent Protein Kinase Type 2
000140176 650_7 $$0EC 2.7.12.2$$2NLM Chemicals$$aMAP Kinase Kinase 4
000140176 650_2 $$2MeSH$$aAnimals
000140176 650_2 $$2MeSH$$aCalcium-Calmodulin-Dependent Protein Kinase Type 2: genetics
000140176 650_2 $$2MeSH$$aCalcium-Calmodulin-Dependent Protein Kinase Type 2: metabolism
000140176 650_2 $$2MeSH$$aDendrites: enzymology
000140176 650_2 $$2MeSH$$aDendrites: genetics
000140176 650_2 $$2MeSH$$aDendrites: metabolism
000140176 650_2 $$2MeSH$$aDishevelled Proteins: genetics
000140176 650_2 $$2MeSH$$aDishevelled Proteins: metabolism
000140176 650_2 $$2MeSH$$aHippocampus: growth & development
000140176 650_2 $$2MeSH$$aHippocampus: metabolism
000140176 650_2 $$2MeSH$$aMAP Kinase Kinase 4: genetics
000140176 650_2 $$2MeSH$$aMAP Kinase Kinase 4: metabolism
000140176 650_2 $$2MeSH$$aMice
000140176 650_2 $$2MeSH$$aMice, Inbred C57BL
000140176 650_2 $$2MeSH$$aNeurites: metabolism
000140176 650_2 $$2MeSH$$aProtein Binding
000140176 650_2 $$2MeSH$$aProto-Oncogene Proteins: genetics
000140176 650_2 $$2MeSH$$aProto-Oncogene Proteins: metabolism
000140176 650_2 $$2MeSH$$aRats
000140176 650_2 $$2MeSH$$aRats, Wistar
000140176 650_2 $$2MeSH$$aReceptors, G-Protein-Coupled: genetics
000140176 650_2 $$2MeSH$$aReceptors, G-Protein-Coupled: metabolism
000140176 650_2 $$2MeSH$$aWnt Proteins: genetics
000140176 650_2 $$2MeSH$$aWnt Proteins: metabolism
000140176 650_2 $$2MeSH$$aWnt Signaling Pathway
000140176 7001_ $$0P:(DE-2719)2810557$$aBernis, María E$$b1$$udzne
000140176 7001_ $$aMcLeod, Faye$$b2
000140176 7001_ $$aPodpolny, Marina$$b3
000140176 7001_ $$aCoullery, Romina P$$b4
000140176 7001_ $$aCasadei, Inelia M$$b5
000140176 7001_ $$aSalinas, Patricia C$$b6
000140176 7001_ $$0P:(DE-HGF)0$$aRosso, Silvana B$$b7$$eCorresponding author
000140176 77318 $$2Crossref$$3journal-article$$a10.1242/jcs.216101$$b : The Company of Biologists, 2018-06-13$$n13$$pjcs216101$$tJournal of Cell Science$$v131$$x0021-9533$$y2018
000140176 773__ $$0PERI:(DE-600)1483099-1$$a10.1242/jcs.216101$$gVol. 131, no. 13, p. jcs216101 -$$n13$$pjcs216101$$q131:13<jcs216101 -$$tJournal of cell science$$v131$$x0021-9533$$y2018
000140176 909CO $$ooai:pub.dzne.de:140176$$pVDB
000140176 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2810557$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b1$$kDZNE
000140176 9131_ $$0G:(DE-HGF)POF3-342$$1G:(DE-HGF)POF3-340$$2G:(DE-HGF)POF3-300$$aDE-HGF$$bForschungsbereich Gesundheit$$lErkrankungen des Nervensystems$$vDisease Mechanisms and Model Systems$$x0
000140176 9131_ $$0G:(DE-HGF)POF3-341$$1G:(DE-HGF)POF3-340$$2G:(DE-HGF)POF3-300$$aDE-HGF$$bForschungsbereich Gesundheit$$lErkrankungen des Nervensystems$$vMolecular Signaling$$x1
000140176 9141_ $$y2018
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