Browse our anti-WNT5B (WNT5B) Antibodies

Mouse (Murine) Wingless-Type MMTV Integration Site Family, Member 5B (WNT5B) interaction partners

1. opposing gradients of Wnt5a and Wnt5b and of their Sfrp inhibitors, together with intercellular signaling via planar cell polarity proteins, polarize node cells along the anterior-posterior axis for breaking of left-right symmetry.

2. Wnt5b activated known calcium-dependent signaling pathways and JNK, a component of the planar cell polarity pathway.

3. Secreted Wnt glycoproteins, expressed by thymic epithelial cells and thymocytes, regulate epithelial Foxn1 expression in both autocrine and paracrine fashions. Wnt molecules therefore provide regulatory signals critical for thymic function.

4. Data indicate that Wnt5a and Wnt5b control the pace of transitions between different chondrocyte zones.

5. Wnt5b may promote adipogenesis in 3T3-L1 cells, at least in part, by antagonizing the canonical Wnt/beta-catenin pathway

6. hCG was found to up-regulate these wnt ligands in mouse mammary gland, independent of the changes in ovarian steroidogenesis

7. this study aimed at defining the expression profile and function of Wnt5a and Wnt5b during adipogenesis by determining their effect on aP2 and PPARgamma expression and assessing the level of beta-catenin translocation in mouse 3T3-L1 preadipocytes.

Xenopus laevis Wingless-Type MMTV Integration Site Family, Member 5B (WNT5B) interaction partners

1. Together these findings provide important and novel insights into the role of canonical Wnt signals during the patterning of vertebrate ectoderm and indicate that Wnt inhibition plays a central role in the process of neural induction.

Human Wingless-Type MMTV Integration Site Family, Member 5B (WNT5B) interaction partners

1. exaggerated WNT-5B expression upon cigarette smoke exposure in the bronchial epithelium of COPD patients leads to TGF-beta/Smad3-dependent expression of genes related to airway remodelling

2. were not able to replicate or further verify the genetic association of polymorphisms in WNT4 and WNT5B with bone mineral density

3. the data suggest that WNT5B induces tube formation by regulating the expression of Snail and Slug proteins through activation of canonical and non-canonical WNT signalling pathways.

4. Noncanonical Wnt signaling via Wnt5a/5b/11 may have role in the pathogenesis of aortic valve calcification.

5. WNT-5B induces IL-6 and CXCL8 secretion in pulmonary fibroblasts.

6. overexpression of WNT5B significantly increased cell proliferation, migration and invasion capacities of the COLO 205 cells in vitro. WNT5B may play an important role in the tumorigenesis of colorectal cancer.

7. results suggest that Wnt5b-associated exosomes promote cancer cell migration and proliferation in a paracrine manner

8. these results suggest that TGF-beta1 stimulates HSC-4 cell invasion through the Slug/Wnt-5b/MMP-10 signalling axis.

9. This study identified WNT5B and CTNNBL1 for peak bone mineral density and body composition in males from the Han Chinese ethnic group.

10. The interaction between Wnt isoforms and their LRP6 cognate receptor depends on the jutting loop present in Wnt3a but absent in Wnt5b.

11. Results demonstrate that the Wnt5B pathway may play an important role in atypical teratoid rhabdoid tumor biology.

12. Report increased Wnt5b levels in adriamycin treated liver cancer stem cells within 4h of treatment.

13. This study shows that the WNT5B germline variant rs2010851 was significantly identified as a stage-dependent prognostic marker for CC patients after 5-fluorouracil-based adjuvant therapy.

14. WNT5B is elevated in both in the tumor and the patients' serum from triple negative breast cancer.

15. Knocking down Wnt5b expression reduced phospho-PKCA levels and cell migration.

16. Ursolic acid suppressed the expression of Wnt5alpha/beta and beta-catenin, inducing apoptosis in prostate cancer cells.

17. These results indicate that Wnt5b is involved in the migration ability of OSCC cells through active Cdc42 and RhoA.

18. WNT3 and WNT5B are critical factors, secreted from mesenchymal cancer cells, for instigating the epithelial cancer cell invasion.

19. TGF-beta/Smad, integrin/integrin-linked kinase (ILK) and wnt/beta-catenin signaling pathways are involved in epithelial to mesenchymal transition in human renal fibrogenesis.

20. Differentiation paralleled the activation of Wnt5/Calmodulin signalling by autocrine/paracrine intense secretion of Wnt5a and Wnt5b

Zebrafish Wingless-Type MMTV Integration Site Family, Member 5B (WNT5B) interaction partners

1. the chaperon Wls and its ligands Wnt9a and Wnt5b are expressed in the ectoderm, whereas juxtaposed chondrocytes express Frzb and Gpc4.

2. disruption of wls resulted in a significant loss of craniofacial bone, whereas lack of gpc4, wnt5b and wnt9a resulted in severely delayed endochondral ossification.

3. novel mechanism for Wnt5b and Gpc4 regulation of chondrocyte behavior that is independent of the core Wnt/PCP molecules and differs from their collaborative action of controlling cell movements during gastrulation

4. In embryos overexpressing lbx1b, wnt5b, a ligand of the non-canonical Wnt/planar cell polarity (PCP) pathway, was significantly downregulated.

5. Swap70b and Def6a delineate Wnt11 and Wnt5b signalling pathways and have roles in convergent and extension cell movement during zebrafish gastrulation

6. CNBP up-regulates tbx2b and smarca5, and down-regulates wnt5b gene expression.

7. def6 morphants phenocopy Wnt5b mutants and ectopic overexpression of def6 essentially rescues Wnt5b morphants, indicating a novel role for def6 as a central GEF downstream of Wnt5b signaling

8. identify rgs3 as having an overlapping expression pattern with wnt5b in zebrafish and reveal that individual knockdown of either rgs3 or wnt5b gene function produces similar somite patterning defects.

9. Data suggest that full-length Ryk conveys Wnt5b signals in a directional manner during gastrulation.

10. Ppt/Wnt5 has a role in regulating cell shape and movement during zebrafish gastrulation

11. Data suggest that the Wnt-5 loss-of-function defect is consistent with calcium modulation having an antagonistic interaction with Wnt/beta-catenin signaling.

12. conserved role of a Wnt5/Fz2 signaling pathway in islet formation during pancreatic development.