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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 (Montrer FZD2 Protéines) or Tc-fz4 RNAi knockdowns.
The screening of candidate genes namely NDP (Montrer NDP Protéines), FZD4 and TSPAN12 (Montrer TSPAN12 Protéines) led to the identification of six major coding region variants in 36 ROP (Montrer STXBP1 Protéines) probands.
Seven novel mutations found in this study have broadened the spectrum of mutations in FZD4 known to cause familial exudative vitreoretinopathy (FEVR (Montrer NDP Protéines)), providing a deeper understanding of this disease. The results show that mutations in FZD4 are associated with the phenotypes of retinal folds or ectopic macula in FEVR (Montrer NDP Protéines)
Three affected individuals within a family with FEVR (Montrer NDP Protéines) presented with variable disease severity. All three affected family members harboured mutation c.349T>C (p.Cys117Arg) in FZD4.
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 (Montrer WNT2 Protéines) signaling
Study shows that WNT5A (Montrer WNT5A Protéines) stimulates dimerization of membrane-anchored FZD4 CRDs and oligomerization of full-length FZD4, which requires the integrity of CRD (Montrer CRX Protéines) palmitoleoyl-binding residues. These results suggest that FZD receptors may form signalosomes in response to Wnt (Montrer WNT2 Protéines) binding through the CRDs and that the Wnt (Montrer WNT2 Protéines) palmitoleoyl group is important in promoting these interactions.
FZD4 down-regulation leads to loss of WNT (Montrer WNT2 Protéines)/beta-catenin (Montrer CTNNB1 Protéines) 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 (Montrer WNT2 Protéines)/beta-catenin (Montrer CTNNB1 Protéines) signaling pathway via downregulated Frizzled4.
Among the detected mutations, LRP5 (Montrer LRP5 Protéines) accounted for the largest proportion with a mean mutation rate of 16.1% (5/31, 16.1%), followed by NDP (Montrer NDP Protéines) (3/31, 9.7%), FZD4 (2/31, 6.5%), TSPAN12 (Montrer TSPAN12 Protéines) (1/31, 3.2%), and KIF11 (Montrer KIF11 Protéines) (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.
A splice variant of the Frizzled-4 receptor modulates Wnt (Montrer WNT2 Protéines) 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 (Montrer NDP Protéines)/Fzd4 axis as an endogenous anti-tumor signal in the preneoplastic niche.
Fzd4 and Fzd6 (Montrer FZD6 Protéines) genes have a deep patterning effect on arterial vessel morphogenesis that may determine its functional efficiency
Study identified a novel Wnt5a (Montrer WNT5A Protéines)/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 (Montrer NDP Protéines)/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 (Montrer WNT2 Protéines)/planar cell polarity signaling.
Frizzled4 wnt (Montrer WNT2 Protéines) receptors are significantly increased in pathological neovascularization in a mouse model of oxygen-induced proliferative retinopathy.
targeted inactivation of the TSK (Montrer FBN1 Protéines) gene in mice causes expansion of the ciliary body and up-regulation of Wnt2b (Montrer WNT2B Protéines) 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 (Montrer FZD8 Protéines) 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