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Wnt16 controls a novel genetic regulatory network required for HSC (show FUT1 ELISA Kits) specification
genomic analysis of conserved sequences between human, rat, and zebrafish WNT16
Wnt16 Is Associated with Age-Related Bone Loss and Estrogen Withdrawal in Murine Bone
Describe TGFbeta (show TGFB1 ELISA Kits)-Wnt16-Notch (show NOTCH1 ELISA Kits) signaling conduit in the chondrocyte-like transformation of VSMCs and identify endogenous TGFbeta (show TGFB1 ELISA Kits) activity in MGP (show MGP ELISA Kits)-null VSMCs as a critical mediator of chondrogenesis.
Wnt5a (show WNT5A ELISA Kits) abrogated the inhibitory effects of Wnt16 on Rankl (show TNFSF11 ELISA Kits)-induced osteoclastogenesis
These findings suggest that WNT16 acting via canonical WNT (show WNT2 ELISA Kits) signaling regulates mechanical strain-induced periosteal bone formation and bone size.
Osteoblast-derived WNT16 is a previously unreported key regulator of osteoclastogenesis and fracture susceptibility.
Wnt16 is involved in intramembranous ossification and suppresses osteoblast differentiation through the Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) pathway.
Study revealed new domains of expression for Wnt2 (show WNT2 ELISA Kits), Wnt2b (show WNT2B ELISA Kits), Wnt5b (show WNT5B ELISA Kits), Wnt6 (show WNT6 ELISA Kits), Wnt7b (show WNT7B ELISA Kits), Wnt9a (show WNT9A ELISA Kits), Wnt10a (show WNT10A ELISA Kits), Wnt10b (show WNT10B ELISA Kits), Wnt11 (show WNT11 ELISA Kits) and Wnt16, in the limb.
MicroRNA-374b Suppresses Proliferation and Promotes Apoptosis in T-cell Lymphoblastic Lymphoma by Repressing AKT1 (show AKT1 ELISA Kits) and Wnt-16
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.
ALL cells expressing WNT16 are sensitive to endoplasmic reticulum stress, and show enhanced killing after addition of chloroquine.
loss of endogenous WNT16 results specifically in cortical bone loss, whereas overexpression of WNT16 surprisingly increases mainly trabecular bone mass.
variants at WNT16 were more strongly related to upper limb-bone mineral density, than to bone mineral density at the other sites.
Increased translation of WNT16 can thus lead to an increased inhibitory action of WNT16 on canonical WNT (show WNT2 ELISA Kits) signaling.
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.
Estrogen/progesterone treatment of mature myometrial cells induced expression of WNT11 (show WNT11 ELISA Kits) and WNT16, which remained constitutively elevated in leiomyoma tissues.
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.
wingless-type MMTV integration site family, member 16
, protein Wnt-16
, protein Wnt-16-like
, wingless-type MMTV integration site family member 16
, wingless-type MMTV integration site family member 16b
, wingless-related MMTV integration site 16