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miR-125b/miR-20b and Wnt signalling have roles in glioblastoma phenotypes in a pathway that involves FZD6
Study reports a novel pathogenic variant of the FZD6 gene in autosomal recessive nonsyndromic congenital nail disorder in consanguineous Iranian family.
In this paper we report 3 further families with mutations in FZD6 causing Isolated recessive nail dysplasia.
monomeric rather than dimeric form is active signal initiating unit of the receptor complex; constitutive signaling to ERK1/2 can be affected by modulating the dimeric status
the FZD6-fibronectin actin axis identified in our study could be exploited for drug development in highly metastatic forms of breast cancer
we found that FZD6 expression was negatively regulated by miR199a5p
The rs3808553 of FZD6 is obviously associated with neural tube defects in Han population of northern China
It is associated with poor prognosis in glioblastoma patients.
This study confirms our speculation that down-regulation of FZD6 by beta-Carotene is causally related to the observed up-regulation of cancer related genes
DVL is a master regulator of FZD6/G-protein signaling
FZD6 should be screened for pachyonychia congenita as it is a candidate gene for hereditary nail dysplasias.
sequence analysis revealed a novel homozygous missense mutation (c.1266G>A; p.Gly422Asp) located in the transmembrane domain of the protein FZD6 in individuals of a consanguineous family exhibiting features of nail dysplasia
The present results emphasize the role of FZD6 mutation in Wnt pathways in nail development.
When transplanted into immunodeficient mice, neuroblastoma cells expressing the Fzd6 marker grow more aggressively than their Fzd6 negative counterparts. Fzd6 is a new surface marker of aggressive neuroblastoma cells with stem cell-like features.
This study demonstrates that rare nonsynonymous variants in FZD6 may contribute to NTDs in humans and enlarges the spectrum of mutations that link PCP pathway to Neural tube defects (NTDs).
The current study provides insight into the global changes in gene transcription mediated by chr-ECS and suggests that Fzd6 signaling could represent a novel target for development of novel antidepressants.
Mutations in this gene cause nail dysplasia. Review.
FZD6 mutations can result in severe defects in nail and claw formation through reduced or abolished membranous FZD(6) levels and several nonfunctional WNT-FZD pathways.
Frizzled 6 (HFz6) has a role as a negative regulator of the canonical Wnt. beta-catenin signaling cascade
These results suggested that activation of Wnt4/Fzd6 signaling through a "beta-catenin-independent" pathway played a role in proliferation and survival of the pituitary adenoma cells.
Fzd4 and Fzd6 genes have a deep patterning effect on arterial vessel morphogenesis that may determine its functional efficiency
Eliminating Fz6 in most hair follicle cells or in the inter-follicular epidermis at E15.5 suggests that planar cell polarity signaling in developing follicles is not required to maintain their orientation.
Data show that Wnt receptor, Frizzled-6 (Fzd6) -/- hematopoietic stem/progenitor cell (HSPC) exhibit poor emergency hematopoiesis.
Fz3 and Fz6 have partly interchangeable roles in tissue polarity signaling for epithelial orientation and axon growth and guidance
Fzd6-mediated Wnt signaling likely regulates the overall differentiation process of nail/claw formation.
Our results support a role of miR-194 in liver tumorigenesis through its endogenous target Fzd6.
The time course of local hair follicle refinement and the resulting evolution of a montage of competing patterns in Fz6(-/-) skin, is defined.
Downregulated by dietary beta-carotene in lungs of knockout Bcmo1-deficient mice.
Fzd3 and Fzd6 deficiency results in a severe midbrain morphogenesis defect.
Fz6 is expressed in the skin and hair follicles, and targeted deletion of the Fz6 gene produces stereotyped whorls on the hind feet, variable whorls and tufts on the head, and misorientation of hairs on the torso.
In the inner ear of a Vangl2 mutant (Looptail; Lp), Fz3 and Fz6 proteins accumulate to normal levels but do not localize correctly at the cell surface.
Elimination of Fzd6 expression by crossing into Fzd6(-/-) mice significantly delays development of chronic lymphocytic leukemia in this model.
This gene represents a member of the 'frizzled' gene family, which encode 7-transmembrane domain proteins that are receptors for Wnt signaling proteins. The protein encoded by this family member contains a signal peptide, a cysteine-rich domain in the N-terminal extracellular region, and seven transmembrane domains, but unlike other family members, this protein does not contain a C-terminal PDZ domain-binding motif. This protein functions as a negative regulator of the canonical Wnt/beta-catenin signaling cascade, thereby inhibiting the processes that trigger oncogenic transformation, cell proliferation, and inhibition of apoptosis. Alternative splicing results in multiple transcript variants, some of which do not encode a protein with a predicted signal peptide.
, frizzled homolog 6
, frizzled 6
, frizzled 6, seven transmembrane spanning receptor
, seven transmembrane helix receptor
, involved in Wnt signaling, encoding a Wnt receptor