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there was a significant difference in the genotypic frequencies of rs2707466 between hypertrophic and atrophic hip OA in males, with overrepresentation of G alleles in the hypertrophic phenotype. An association in the same direction was observed between these alleles and the type of knee OA, with G alleles being more common in the hypertrophic than in atrophic knee phenotypes
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WNT16B recognizes cancer cell surface receptors including frizzled (FZD) 3/4/6, a process enhanced by SFRP2, coordinated by the co-receptor LRP6 but subject to abrogation by DKK1.
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the upregulation of autophagy-related gene (Atg) and wingless/int1 (Wnt) signaling during BMP-2-mediated human osteoblastic differentiation, was examined.
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PRKX, WNT3 and WNT16 genes, belonging to the WNT signaling pathway, are involved in the tumorigenic process of nodular basal cell carcinoma
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ThE findingS suggests that WNT16 might be an important genetic factor in determining peak bone mass acquisition.
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Although in vitro studies demonstrated no differences in expressions of wild-type and mutant forms of IDUA and WNT16B proteins, in silico analyses predicts that WNT16 rs2707466 directly abolishes a phosphorylation site, which could cause a deleterious effect on WNT16 protein.
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MicroRNA-374b Suppresses Proliferation and Promotes Apoptosis in T-cell Lymphoblastic Lymphoma by Repressing AKT1 and Wnt-16
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Data indicate that WNT16 is critical for positive regulation of both cortical and trabecular bone mass and structure. WNT16-TG mice exhibited significantly higher whole-body areal bone mineral density and bone mineral content.
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ALL cells expressing WNT16 are sensitive to endoplasmic reticulum stress, and show enhanced killing after addition of chloroquine.
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loss of endogenous WNT16 results specifically in cortical bone loss, whereas overexpression of WNT16 surprisingly increases mainly trabecular bone mass.
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Describe TGFbeta-Wnt16-Notch signaling conduit in the chondrocyte-like transformation of VSMCs and identify endogenous TGFbeta activity in MGP-null VSMCs as a critical mediator of chondrogenesis.
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variants at WNT16 were more strongly related to upper limb-bone mineral density, than to bone mineral density at the other sites.
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Osteoblast-derived WNT16 is a previously unreported key regulator of osteoclastogenesis and fracture susceptibility.
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Increased translation of WNT16 can thus lead to an increased inhibitory action of WNT16 on canonical WNT signaling.
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Common missense polymorphisms of the WNT16 gene are associated with bone mineral density at the hip, calcaneal ultrasound and the buckling ratio of the femoral neck, as well as with hip fractures in individuals under 80 years of age.
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Estrogen/progesterone treatment of mature myometrial cells induced expression of WNT11 and WNT16, which remained constitutively elevated in leiomyoma tissues.
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results suggest synergistic effects of WNT16a insertion and the at-risk 'T' allele of TCF7L2 (rs7903146) for elevating the expression of TCF7L2 in human pancreas which may affect the regulation of downstream target genes involved in the development of T2D
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Analyses of femoral neck BMD also supported association with SNPs in WNT16 and ESR1/C6orf97
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Treatment-induced damage to the tumor microenvironment promotes prostate cancer therapy resistance through WNT16B.
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these findings postulate that the WNT16/C7orf58 locus contains complex patterns of genetic variation, which play an important role in peak bone mass accrual and may likely impact BMD determination at later life.
