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This paper reports a novel skull phenotype in a ciliopathic mutant mouse in which only a single calvarial bone plate encases the forebrain in mice lacking Fuz, an essential regulator of ciliogenesis.
Fuzzy appears to control subcellular localization of the core PCP protein Dishevelled, recruiting it to Rab8-positive vesicles and to the basal body and cilium. We show that loss of Fuzzy results in inhibition of PCP signaling
Using the ciliopathic Fuz mutant mouse, we find that high arched palate does not, as commonly suggested, arise from midface hypoplasia; rather, increased neural crest expands the maxillary primordia.
Data report the dynamic expression of another planar cell polarity gene, Fuzzy, during neural tube formation in mice.
The data demonstrate a new model for coordination of Hh and Wnt signaling and reveal a Fuz-dependent negative feedback loop controlling Wnt/beta-catenin signaling.
Data show that the functions of both Inturned and Fuzzy in neural tube patterning are dependent on the presence of cilia.
Fuz controls the morphogenesis and differentiation of hair follicles through the formation of primary cilia.
Fuz plays an important role in cilia formation, Hh signal transduction, and embryonic development in mammals.
results in vitro show that FUZ is responsible for non-small-cell lung cancer (NSCLC) progression and metastasis, suggesting that FUZ can be a potential therapeutic target for NSCLC.
Data propose that mutations in Fuzzy may account for a subset of neural tube defects in humans.
This gene encodes a planar cell polarity protein that is involved in ciliogenesis and directional cell movement. Knockout studies in mice exhibit neural tube defects and defective cilia, and mutations in this gene are associated with neural tube defects in humans. Alternatively spliced transcript variants have been found for this gene.
protein fuzzy homolog
, fuzzy homolog
, fuzzy homolog (Drosophila)