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In this paper we report 3 further families with mutations in FZD6 causing Isolated recessive nail (show CD244 Proteins) 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
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 (show CD244 Proteins) 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 (show CD244 Proteins) dysplasia
The present results emphasize the role of FZD6 mutation in Wnt (show WNT2 Proteins) pathways in nail (show CD244 Proteins) development.
Fzd4 (show FZD4 Proteins) 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 (show PSMA7 Proteins)) exhibit poor emergency hematopoiesis.
Fz3 (show FZD3 Proteins) and Fz6 have partly interchangeable roles in tissue polarity signaling for epithelial orientation and axon growth and guidance
Fzd6-mediated Wnt (show WNT2 Proteins) signaling likely regulates the overall differentiation process of nail (show CD244 Proteins)/claw formation.
Our results support a role of miR (show MLXIP Proteins)-194 in liver tumorigenesis through its endogenous target Fzd6.
FZD6 mutations can result in severe defects in nail (show CD244 Proteins) and claw formation through reduced or abolished membranous FZD(6) levels and several nonfunctional WNT (show WNT2 Proteins)-FZD pathways.
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 (show BCMO1 Proteins)-deficient mice.
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