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FZD6 is highly expressed in liver cancer cells and liver tumor-initiating cells.FZD6 is required for liver tumor-initiating cells self-renewal.LncFZD6 interacts and recruits BRG1 to FZD6 promoter to initiate transcription.
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miR-125b/miR-20b and Wnt signalling have roles in glioblastoma phenotypes in a pathway that involves FZD6
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Study reports a novel pathogenic variant of the FZD6 gene in autosomal recessive nonsyndromic congenital nail disorder in consanguineous Iranian family.
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In this paper we report 3 further families with mutations in FZD6 causing Isolated recessive nail dysplasia.
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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
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the FZD6-fibronectin actin axis identified in our study could be exploited for drug development in highly metastatic forms of breast cancer
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we found that FZD6 expression was negatively regulated by miR199a5p
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The rs3808553 of FZD6 is obviously associated with neural tube defects in Han population of northern China
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It is associated with poor prognosis in glioblastoma patients.
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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
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DVL is a master regulator of FZD6/G-protein signaling
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FZD6 should be screened for pachyonychia congenita as it is a candidate gene for hereditary nail dysplasias.
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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
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The present results emphasize the role of FZD6 mutation in Wnt pathways in nail development.
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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.
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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).
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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.
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Mutations in this gene cause nail dysplasia. Review.
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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.
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Frizzled 6 (HFz6) has a role as a negative regulator of the canonical Wnt. beta-catenin signaling cascade
