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Knockdown of Tc-fz1 alone interfered with the formation of the proximo-distal and the dorso-ventral axes during leg development, whereas no effect was observed with single Tc-fz2 (show FZD2 Proteins) or Tc-fz4 RNAi knockdowns.
The findings in this family support the concept that some mutated FZD4 alleles can be associated with recessive rather than dominant disease.
novel role of let-7b/Fzd4 axis through wnt (show WNT2 Proteins) signaling
Study shows that WNT5A (show WNT5A Proteins) stimulates dimerization of membrane-anchored FZD4 CRDs and oligomerization of full-length FZD4, which requires the integrity of CRD (show CRX Proteins) palmitoleoyl-binding residues. These results suggest that FZD receptors may form signalosomes in response to Wnt (show WNT2 Proteins) binding through the CRDs and that the Wnt (show WNT2 Proteins) palmitoleoyl group is important in promoting these interactions.
FZD4 down-regulation leads to loss of WNT (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signal activity and subsequently to reduced alveolar epithelial cell wound repair capacity and impaired expression of elastogenic components.
his study showed that Let7b modulates the proliferation, invasiveness, and migration of liver cancer cell and reduces the proportion of cancer stem cells in liver cancer cell by inhibiting Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signaling pathway via downregulated Frizzled4.
Among the detected mutations, LRP5 (show LRP5 Proteins) accounted for the largest proportion with a mean mutation rate of 16.1% (5/31, 16.1%), followed by NDP (show NDP Proteins) (3/31, 9.7%), FZD4 (2/31, 6.5%), TSPAN12 (show TSPAN12 Proteins) (1/31, 3.2%), and KIF11 (show KIF11 Proteins) (1/31, 3.2%). All the novel changes were predicted to be pathogenic by a series of bioinformatics analyses.
human FZD4 assembles-in a DVL-independent manner-with Galpha12/13 but not representatives of other heterotrimeric G protein subfamilies.
Several novel mutations (missense, non-stop (show USP22 Proteins) and insertion) were detected in the coding regions of FZD4, TSPAN12 (show TSPAN12 Proteins) and ZNF408 (show ZNF408 Proteins) genes among the unrelated familial exudative vitreoretinopathy probands. The mutations in FZD4 and TSPAN12 (show TSPAN12 Proteins) were involved in autosomal dominant and autosomal recessive families and further validates the involvement of these gene in exudative vitreoretinopathy development.
Two were novel mutations: p.E134* and p.T503fs of FZD4 lead to the loss of FZD4 activity.
Letter: FZD4+ and FZD4- melanocytes were significantly lower in hair follicles of patients with rhododenol-induced leukoderma.
A splice variant of the Frizzled-4 receptor modulates Wnt (show WNT2 Proteins) signalling in a dose-dependent, biphasic manner.
These data expose a stromal component that regulates the earliest stages of tumorigenesis in the cerebellum, and a novel role for the Norrin (show NDP Proteins)/Fzd4 axis as an endogenous anti-tumor signal in the preneoplastic niche.
Fzd4 and Fzd6 (show FZD6 Proteins) genes have a deep patterning effect on arterial vessel morphogenesis that may determine its functional efficiency
Study identified a novel Wnt5a (show WNT5A Proteins)/Fzd4 signaling pathway that contributes to the regulation of dendrite morphogenesis
These results question the conclusion that a dominant-negative mechanism would explain the dominance of the mutant L501fsX533 Fz4 allele in the transmission of a form of Familial exudative vitreoretinopathy.
The data reveal both cell-autonomous and cell-nonautonomous effects, and they imply a central role for Norrin (show NDP Proteins)/Fz4 signaling in central nervous system vascular development and in the maintenance of the blood brain barrier/blood retina barrier state.
Frizzled 4 regulates arterial network organization through noncanonical Wnt (show WNT2 Proteins)/planar cell polarity signaling.
Frizzled4 wnt (show WNT2 Proteins) receptors are significantly increased in pathological neovascularization in a mouse model of oxygen-induced proliferative retinopathy.
targeted inactivation of the TSK (show FBN1 Proteins) gene in mice causes expansion of the ciliary body and up-regulation of Wnt2b (show WNT2B Proteins) and Fzd4 expression in the developing peripheral eye
These results demonstrate that FZD4 is required for physiological and pathologic angiogenesis in the retina and for regulation of retinal endothelial cell differentiation.
A major role for frizzled 4 and frizzled 8 (show FZD8 Proteins) in controlling ureteric growth in the developing kidney.
This gene is a member of the frizzled gene family. Members of this family encode seven-transmembrane domain proteins that are receptors for the Wingless type MMTV integration site family of signaling proteins. Most frizzled receptors are coupled to the beta-catenin canonical signaling pathway. This protein may play a role as a positive regulator of the Wingless type MMTV integration site signaling pathway. A transcript variant retaining intronic sequence and encoding a shorter isoform has been described, however, its expression is not supported by other experimental evidence.
, frizzled homolog 1
, frizzled homolog 4
, WNT receptor frizzled-4
, frizzled 4, seven transmembrane spanning receptor
, frizzled receptor 4
, frizzled 4 protein