% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Ferrari:140176,
author = {Ferrari, María E and Bernis, María E and McLeod, Faye and
Podpolny, Marina and Coullery, Romina P and Casadei, Inelia
M and Salinas, Patricia C and Rosso, Silvana B},
title = {{W}nt7b signalling through {F}rizzled-7 receptor promotes
dendrite development by coactivating {C}a{MKII} and {JNK}.},
journal = {Journal of cell science},
volume = {131},
number = {13},
issn = {0021-9533},
address = {Cambridge},
publisher = {Company of Biologists Limited},
reportid = {DZNE-2020-06498},
pages = {jcs216101},
year = {2018},
abstract = {The 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.},
keywords = {Animals / Calcium-Calmodulin-Dependent Protein Kinase Type
2: genetics / Calcium-Calmodulin-Dependent Protein Kinase
Type 2: metabolism / Dendrites: enzymology / Dendrites:
genetics / Dendrites: metabolism / Dishevelled Proteins:
genetics / Dishevelled Proteins: metabolism / Hippocampus:
growth $\&$ development / Hippocampus: metabolism / MAP
Kinase Kinase 4: genetics / MAP Kinase Kinase 4: metabolism
/ Mice / Mice, Inbred C57BL / Neurites: metabolism / Protein
Binding / Proto-Oncogene Proteins: genetics / Proto-Oncogene
Proteins: metabolism / Rats / Rats, Wistar / Receptors,
G-Protein-Coupled: genetics / Receptors, G-Protein-Coupled:
metabolism / Wnt Proteins: genetics / Wnt Proteins:
metabolism / Wnt Signaling Pathway / Dishevelled Proteins
(NLM Chemicals) / Dvl1 protein, mouse (NLM Chemicals) / Fzd7
protein, mouse (NLM Chemicals) / Proto-Oncogene Proteins
(NLM Chemicals) / Receptors, G-Protein-Coupled (NLM
Chemicals) / Wnt Proteins (NLM Chemicals) / Wnt7b protein,
mouse (NLM Chemicals) / Calcium-Calmodulin-Dependent Protein
Kinase Type 2 (NLM Chemicals) / MAP Kinase Kinase 4 (NLM
Chemicals)},
cin = {AG Tamgüney 2},
ddc = {570},
cid = {I:(DE-2719)1013022},
pnm = {342 - Disease Mechanisms and Model Systems (POF3-342) / 341
- Molecular Signaling (POF3-341)},
pid = {G:(DE-HGF)POF3-342 / G:(DE-HGF)POF3-341},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:29898920},
doi = {10.1242/jcs.216101},
url = {https://pub.dzne.de/record/140176},
}