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anti-Human FZD4 Antibodies:
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Human Monoclonal FZD4 Primary Antibody for IHC (fro), FACS - ABIN2689205
Ells, Guernsey, Wallace, Zheng, Vincer, Allen, Ingram, DaSilva, Siebert, Sheidow, Beis, Robitaille: Severe retinopathy of prematurity associated with FZD4 mutations. in Ophthalmic genetics 2010
Show all 8 Pubmed References
Cow (Bovine) Polyclonal FZD4 Primary Antibody for IHC, WB - ABIN2776715
Dufourcq, Leroux, Ezan, Descamps, Lamazière, Costet, Basoni, Moreau, Deutsch, Couffinhal, Duplàa: Regulation of endothelial cell cytoskeletal reorganization by a secreted frizzled-related protein-1 and frizzled 4- and frizzled 7-dependent pathway: role in neovessel formation. in The American journal of pathology 2008
Show all 4 Pubmed References
Human Monoclonal FZD4 Primary Antibody for CyTOF, FACS - ABIN4900304
Baksh, Boland, Tuan: Cross-talk between Wnt signaling pathways in human mesenchymal stem cells leads to functional antagonism during osteogenic differentiation. in Journal of cellular biochemistry 2007
Show all 2 Pubmed References
Human Polyclonal FZD4 Primary Antibody for ELISA, WB - ABIN548187
You, Nguyen, Albers, Lin, Holcombe: Wnt pathway-related gene expression in inflammatory bowel disease. in Digestive diseases and sciences 2008
Human Monoclonal FZD4 Primary Antibody for FACS, ICC - ABIN4898976
Despeaux, Chicanne, Rouer, De Toni-Costes, Bertrand, Mansat-De Mas, Vergnolle, Eaves, Payrastre, Girault, Racaud-Sultan: Focal adhesion kinase splice variants maintain primitive acute myeloid leukemia cells through altered Wnt signaling. in Stem cells (Dayton, Ohio) 2012
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 or Tc-fz4 RNAi knockdowns.
This is the first study to report a group of patients with digenic familial exudative vitreoretinopathy (FEVR). In most affected eyes, the stage was more severe than stage 3. We speculate that the phenotype of FEVR is more severe in patients with digenic rather than monogenic variants of FEVR-related genes.
FzM1.8 is an allosteric agonist of FZD4. In the absence of any WNT ligand, FzM1.8 binds to FZD4, promotes recruitment of heterotrimeric G proteins, and biases WNT signaling toward a noncanonical route that involves PI3K. In colon cancer cells, the FZD4/PI3K axis elicited by FzM1.8 preserves stemness and promotes proliferation of undifferentiated cells.
FZD4 Tyrosine 250(2.39) is crucial for DVL2 interaction and DVL2 translocation to the plasma membrane.
Accessory proteins in Frizzled (FZD) receptor complexes are thought to determine ligand selectivity and signaling amplitude.
FZD4 was confirmed to be a downstream target of miR-505, and found to be up-regulated in cervical cancer patients.
The screening of candidate genes namely NDP, FZD4 and TSPAN12 led to the identification of six major coding region variants in 36 ROP probands.
Seven novel mutations found in this study have broadened the spectrum of mutations in FZD4 known to cause familial exudative vitreoretinopathy (FEVR), 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
Three affected individuals within a family with FEVR 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 signaling
Study shows that WNT5A stimulates dimerization of membrane-anchored FZD4 CRDs and oligomerization of full-length FZD4, which requires the integrity of CRD palmitoleoyl-binding residues. These results suggest that FZD receptors may form signalosomes in response to Wnt binding through the CRDs and that the Wnt palmitoleoyl group is important in promoting these interactions.
FZD4 down-regulation leads to loss of WNT/beta-catenin 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/beta-catenin signaling pathway via downregulated Frizzled4.
Among the detected mutations, LRP5 accounted for the largest proportion with a mean mutation rate of 16.1% (5/31, 16.1%), followed by NDP (3/31, 9.7%), FZD4 (2/31, 6.5%), TSPAN12 (1/31, 3.2%), and KIF11 (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 and insertion) were detected in the coding regions of FZD4, TSPAN12 and ZNF408 genes among the unrelated familial exudative vitreoretinopathy probands. The mutations in FZD4 and TSPAN12 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.
These structural, biophysical and cellular data, map Fz4 and putative Lrp5/6 binding sites to distinct patches on Norrin, and reveal a GAG binding site spanning Norrin and Fz4 cysteine-rich domain.
The relatively high prevalence of the p.[P33S(;)P168S] variant in ROP (retinopathy of prematurity) and intrauterine growth restriction suggests that it also may be a marker for increased risk of developing ROP and preterm birth.
Hnf1beta and Fzd4/Fzd4s appear to be involved in pre-patterning events of the embryonic endoderm that allow pancreas formation in Xenopus.
A splice variant of the Frizzled-4 receptor modulates Wnt signalling in a dose-dependent, biphasic manner.
NORRIN presented to FZD4 further increases cardiomyocyte output via proliferation through the canonical WNT pathway.
results provide functional and biochemical dissection of Fzd4 in Norrin signaling.
FZD4 was upregulated during cyclic mechanical stretch (CMS)-induced osteogenic differentiation, and the JNK signalling pathway was activated. FZD4 knockdown inhibited the mechanical stimuli-induced osteogenesis and JNK activity.
These data expose a stromal component that regulates the earliest stages of tumorigenesis in the cerebellum, and a novel role for the Norrin/Fzd4 axis as an endogenous anti-tumor signal in the preneoplastic niche.
Fzd4 and Fzd6 genes have a deep patterning effect on arterial vessel morphogenesis that may determine its functional efficiency
Study identified a novel Wnt5a/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/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/planar cell polarity signaling.
Frizzled4 wnt receptors are significantly increased in pathological neovascularization in a mouse model of oxygen-induced proliferative retinopathy.
targeted inactivation of the TSK gene in mice causes expansion of the ciliary body and up-regulation of Wnt2b 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 in controlling ureteric growth in the developing kidney.
a Norrin-Fz4 signaling system plays a central role in vascular development in the eye and ear, and ligands unrelated to Wnts can act through Fz receptors
Fzd4 appears to impact the formation of the corpus luteum
Hyperosmotic sucrose and K(+) depletion increased the membrane localization of FZD(4)-GFP, and in parallel triggered fast and almost complete degradation of endogenous dishevelled
sFRP-1 can interact with Wnt receptors Frizzled 4 and 7 on endothelial cells to transduce downstream to cellular machineries requiring Rac-1 activity in cooperation with GSK-3beta
Loss of Fz4 in all endothelial cells disrupts the blood brain barrier in the cerebellum, whereas excessive Fz4 signaling disrupts embryonic angiogenesis.
Data indicate that Norrin multimers and TSPAN12 cooperatively promote multimerization of FZD4 and its associated proteins to elicit physiological levels of signaling.
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