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Wingless-type MMTV integration site family, member 16

The WNT gene family consists of structurally related genes which encode secreted signaling proteins. These proteins have been implicated in oncogenesis and in several developmental processes, including regulation of cell fate and patterning during embryogenesis. This gene is a member of the WNT gene family. It contains two transcript variants diverging at the 5' termini. These two variants are proposed to be the products of separate promoters and not to be splice variants from a single promoter. They are differentially expressed in normal tissues, one of which (variant 2) is expressed at significant levels only in the pancreas, whereas another one (variant 1) is expressed more ubiquitously with highest levels in adult kidney, placenta, brain, heart, and spleen. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: fibrillin-1, AGE, Wnt4, CAN, Wnt3
Papers on Wnt16
Polymorphisms in Wnt signaling pathway genes are associated with peak bone mineral density, lean mass, and fat mass in Chinese male nuclear families.
Zhang et al., Shanghai, China. In Osteoporos Int, Feb 2016
INTRODUCTION: Our objective was to investigate the associations between polymorphisms in WNT4, WNT5B, WNT10B, WNT16, CTNNB1, and CTNNBL1 genes and peak bone mineral density (BMD), lean mass (LM), and fat mass (FM) in young Chinese men.
The bone-sparing effects of estrogen and WNT16 are independent of each other.
Ohlsson et al., Göteborg, Sweden. In Proc Natl Acad Sci U S A, Jan 2016
Wingless-type MMTV integration site family (WNT)16 is a key regulator of bone mass with high expression in cortical bone, and Wnt16(-/-) mice have reduced cortical bone mass.
Osteoblast-specific Overexpression of Human WNT16 Increases both Cortical and Trabecular Bone Mass and Structure in Mice.
Econs et al., United States. In Endocrinology, Dec 2015
Recently, we identified SNPs in WNT16 that were associated with peak BMD in premenopausal women.
MicroRNA-374b Suppresses Proliferation and Promotes Apoptosis in T-cell Lymphoblastic Lymphoma by Repressing AKT1 and Wnt-16.
Cai et al., Tianjin, China. In Clin Cancer Res, Dec 2015
Real-time quantitative PCR and immunohistochemistry (IHC) were applied to detect the expression of miR-374b, AKT1, and Wnt16 in T-LBL samples.
Polymorphisms of the WNT16 gene are associated with the heel ultrasound parameter in young adults.
Rueda-Medina et al., Granada, Spain. In Osteoporos Int, Nov 2015
We investigated the role of WNT16 in bone properties determined using quantitative ultrasound (QUS) on young adults.
Whole-genome sequencing identifies EN1 as a determinant of bone density and fracture.
Richards et al., Montréal, Canada. In Nature, Nov 2015
We also identified a novel low-frequency non-coding variant with large effects on BMD near WNT16 (rs148771817(T), MAF = 1.2%, replication effect size = +0.41 s.d., Pmeta = 1 × 10(-11)).
Genetic Approaches To Identifying Novel Osteoporosis Drug Targets.
Brommage, The Woodlands, United States. In J Cell Biochem, Oct 2015
In addition to the classic Wnt signaling targets DKK1 and sclerostin, LRP4, LRP5/LRP6, SFRP4, WNT16, and NOTUM can potentially be targeted to modulate Wnt signaling.
WNT3 involvement in human bladder exstrophy and cloaca development in zebrafish.
Nordenskjöld et al., Stockholm, Sweden. In Hum Mol Genet, Oct 2015
In total 13 variants were identified in WNT3, WNT6, WNT7A, WNT8B, WNT10A, WNT11, WNT16, FZD5, LRP1 and LRP10 genes and predicted as potentially disease causing, of which seven variants were novel.
A trans-ethnic genome-wide association study identifies gender-specific loci influencing pediatric aBMD and BMC at the distal radius.
Grant et al., Cincinnati, United States. In Hum Mol Genet, Oct 2015
Signals at the CPED1-WNT16-FAM3C locus have been previously associated with BMD at other skeletal sites in adults and children.
Genetics of Bone Mass in Childhood and Adolescence: Effects of Sex and Maturation Interactions.
Grant et al., Philadelphia, United States. In J Bone Miner Res, Sep 2015
In contrast, the sex • SNP interactions for loci near LRP5 and WNT16 uncovered associations that were only in males for total body less head BMC (b = 0.22, p = 4.4 × 10(-4)) and distal radius aBMD (b = 0.27, p = 0.001), respectively.
WNT16-expressing Acute Lymphoblastic Leukemia Cells are Sensitive to Autophagy Inhibitors after ER Stress Induction.
Denko et al., Pátrai, Greece. In Anticancer Res, Sep 2015
Acute lymphoblastic leukemia (ALL) cells with the t(1:19) translocation express the WNT16 gene, which is thought to contribute to transformation.
Identification of IDUA and WNT16 Phosphorylation-Related Non-Synonymous Polymorphisms for Bone Mineral Density in Meta-Analyses of Genome-Wide Association Studies.
Deng et al., New Orleans, United States. In J Bone Miner Res, Sep 2015
IDUA rs3755955 and rs6831280, and WNT16 rs2707466 were associated with BMD phenotypes in each respective stage, and in three stages combined, achieving GWS for both FN-BMD (p = 8.36 × 10(-10) , p = 5.26 × 10(-10) , and p = 3.01 × 10(-10) , respectively) and HIP-BMD (p = 3.26 × 10(-6) , p = 1.97 × 10(-6) , and p = 1.63 × 10(-12) , respectively).
A new WNT on the bone: WNT16, cortical bone thickness, porosity and fractures.
Baron et al., Boston, United States. In Bonekey Rep, 2014
Within the components of WNT signaling, the gene coding for WNT16, one of the 19 WNT ligands of the human genome, has been found strongly associated with specific bone traits such as cortical bone thickness, cortical porosity and fracture risk.
Osteoblast-derived WNT16 represses osteoclastogenesis and prevents cortical bone fragility fractures.
Ohlsson et al., Göteborg, Sweden. In Nat Med, 2014
The WNT16 locus is a major determinant of cortical bone thickness and nonvertebral fracture risk in humans.
Clinical review: Genome-wide association studies of skeletal phenotypes: what we have learned and where we are headed.
Kiel et al., Boston, United States. In J Clin Endocrinol Metab, 2012
Among 59 novel BMD GWAS loci that have not been reported by previous candidate gene association studies, some have been shown to be involved in key biological pathways involving the skeleton, particularly Wnt signaling (AXIN1, LRP5, CTNNB1, DKK1, FOXC2, HOXC6, LRP4, MEF2C, PTHLH, RSPO3, SFRP4, TGFBR3, WLS, WNT3, WNT4, WNT5B, WNT16), bone development: ossification (CLCN7, CSF1, MEF2C, MEPE, PKDCC, PTHLH, RUNX2, SOX6, SOX9, SPP1, SP7), mesenchymal-stem-cell differentiation (FAM3C, MEF2C, RUNX2, SOX4, SOX9, SP7), osteoclast differentiation (JAG1, RUNX2), and TGF-signaling (FOXL1, SPTBN1, TGFBR3).
Treatment-induced damage to the tumor microenvironment promotes prostate cancer therapy resistance through WNT16B.
Nelson et al., Seattle, United States. In Nat Med, 2012
Treatment-induced damage to the tumor microenvironment promotes prostate cancer therapy resistance through WNT16B.
Meta-analysis of genome-wide scans for total body BMD in children and adults reveals allelic heterogeneity and age-specific effects at the WNT16 locus.
Rivadeneira et al., Rotterdam, Netherlands. In Plos Genet, 2012
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.
WNT16 influences bone mineral density, cortical bone thickness, bone strength, and osteoporotic fracture risk.
Lorentzon et al., Montréal, Canada. In Plos Genet, 2012
These results suggest a critical role of Wnt 16 signaling pathway on cortical bone thickness and bone strength determination as well as fracture susceptibility.
WNT16B is a new marker of cellular senescence that regulates p53 activity and the phosphoinositide 3-kinase/AKT pathway.
Pedeux et al., Grenoble, France. In Cancer Res, 2010
study identified WNT16B as a new marker of senescence that regulates p53 activity and the PI3K/AKT pathway and is necessary for the onset of replicative senescence
Variation in WNT genes expression in different subtypes of chronic lymphocytic leukemia.
Shokri et al., Tehrān, Iran. In Leuk Lymphoma, 2009
Results demonstrated significant up-regulation of WNT-3, WNT-4, WNT-5B, WNT-7B, WNT-9A, WNT-10A, and WNT-16B in patients with CLL compared to normal subjects.
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