Browse our anti-WNT9B (WNT9B) Antibodies

Human Wingless-Type MMTV Integration Site Family, Member 9B (WNT9B) interaction partners

1. Our study further supports the involvement of WNT9B as a cleft susceptibility gene in Brazilian families experiencing NSCL+/-P. Although additional studies are still necessary to unveil the exact mechanism by which WNT genes would contribute to NSCL+/-P, allelic polymorphisms in these genes and their interactions may partly explain the variance of individual susceptibility to NSCL+/-P.

2. Multi-layered mutation in hedgehog-related genes in Gorlin syndrome may affect the phenotype

3. This association study successfully identified two susceptibility Single Nucleotide Polymorphisms, (WNT9B and PBX1) associated with Mayer-Rokitansky-Kuster-Hauser syndrome risk, both separately and interactively.

4. Genome association study shows a highly conserved 32 kb intergenic region containing regulatory elements between WNT3 and WNT9B in patients with classic bladder exstrophy.

5. results indicate that mutations in the coding sequence of WNT9B are not responsible for Mullerian duct abnormalities in the Chinese population

6. Two novel mutations (a missense mutation in exon 1, and one in the 3-UTR) may be pathogenic variants in Mayer-Rokitansky-Kuster-Hauser syndrome patients and warrant further functional study.

7. secretion of WNT2B and WNT9B and stabilization of beta-catenin (CTNNB1) upon virus infection negatively regulate expression of representative inducible genes IFNB1, IFIT1 and TNF in a CTNNB1-dependent effector mechanism

8. The signals from the stromal fibroblasts cooperate with Wnt9b to promote differentiation of the progenitor cells.

9. Mutations in the coding sequence of WNT4, WNT5A, WNT7A, and WNT9B are not responsible for the Mayer-Rokitansky-Kuster-Hauser syndrome.

Zebrafish Wingless-Type MMTV Integration Site Family, Member 9B (WNT9B) interaction partners

1. Ancestral roles for Wnt9s in early patterning of neural/oral-pharyngeal ectoderm and mesendoderm derivatives.

2. These analyses suggest that in zebrafish, as in humans, wnt9b plays distinct roles in directing morphogenetic movements of developing branchial arch elements.

Mouse (Murine) Wingless-Type MMTV Integration Site Family, Member 9B (WNT9B) interaction partners

1. Data indicate that mutations in wingless-type MMTV integration site family, member 9B protein (WNT9B) were frequently associated with Mayer-Rokitansky-Kuster-Hauser syndrome (MRKHS).

2. Epigenetic mechanism causes Wnt9b deficiency and nonsyndromic cleft lip and palate in the A/WySn mouse strain.

3. Expression of Wnt9b in Six2-positive cells disrupts cell fate decisions in the kidney and the gastrointestinal tract.

4. Epithelial Wnt7b and Wnt9b as possible ligands of Fzd1-mediated beta-catenin (Ctnnb1)-dependent (canonical) Wnt signaling in the undifferentiated ureteric mesenchyme

5. Study has identified a previously unknown regulatory link between WNT9B and FGF signaling during lip and upper jaw development.

6. Notch pathway activation can replace the requirement for Wnt4 and Wnt9b in mesenchymal-to-epithelial transition of nephron stem cells

7. wnt9b signaling regulates stem cell proliferation and differention in the developing kidney depending on the activity of the transcription factor Six2 in the responding cell.

8. transgenic overexpression of Wnt9b in the ureteric bud causes reduced branching in multiple founder lines.

9. expression in most but not all tissues of the 16.5-day embryo; no significant elevation of Wnt9b expression was detected in 29 mouse mammary tumor virus-induced tumors

10. Wnt9b is a common organizing signal regulating diverse components of the mammalian urogenital system.

11. Signals through the canonical Wnt signaling pathway to regulate midfacial development and lip fusion.

12. The noncomplementation of clf1 and Wnt9b- confirms that clf1 is a mutation of the Wnt9b gene.

13. Findings show that Wnt9b, produced by the kidney collecting ducts, nonautonomously regulates morphogenesis of the developing kidney tubules.