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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 (zeige BMP1 Proteine) protein Dishevelled (zeige DVL2 Proteine), recruiting it to Rab8 (zeige RAB8A Proteine)-positive vesicles and to the basal body and cilium. We show that loss of Fuzzy results in inhibition of PCP (zeige BMP1 Proteine) 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.
The data demonstrate a new model for coordination of Hh and Wnt (zeige WNT2 Proteine) signaling and reveal a Fuz-dependent negative feedback loop controlling Wnt (zeige WNT2 Proteine)/beta-catenin (zeige CTNNB1 Proteine) signaling.
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.
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)