Disease relevance of Wnt5b

• The cells were smaller and grew to a higher density than cells containing a control retrovirus or cells expressing Wnt-4 or Wnt-5b [1].

High impact information on Wnt5b

• Furthermore, overexpression of the Wnt5b gene in preadipocytes resulted in the promotion of adipogenesis and the enhancement of adipocytokine-gene expression [2].
• Subsequent in vitro experiments identified the fact that expression of the Wnt5b gene was increased at an early phase of adipocyte differentiation in mouse 3T3-L1 cells [2].
• We have studied the roles of two members of the Wnt family, Wnt5a and Wnt5b in long bone development [3].
• Wnt5a and Wnt5b exhibit distinct activities in coordinating chondrocyte proliferation and differentiation [3].
• No such compensation was apparent in aged myoblasts and in fact, both Wnt5b and Wnt10b were down-regulated [4].

Biological context of Wnt5b

• To elucidate the functional roles of Wnt5b in adipogenesis, we characterized gene expression profiles in Wnt5b overexpressing 3T3-L1 cells using microarray analysis [5].
• Comparative genomics on Wnt5a and Wnt5b genes [6].
• Here, we identified and characterized rat Wnt5a and Wnt5b genes by using bioinformatics [6].

Anatomical context of Wnt5b

• Wnt5b and Wnt6 exhibit restricted expression in the epithelium of the esophagus [7].

Regulatory relationships of Wnt5b

• Wnt5b partially inhibits canonical Wnt/beta-catenin signaling pathway and promotes adipogenesis in 3T3-L1 preadipocytes [5].

Other interactions of Wnt5b

• Finally, Wnt-2, Wnt-4 and Wnt-5b were shown to be regulated by ovarian hormones [8].
• These findings indicate that Wnt5b may promote adipogenesis in 3T3-L1 cells, at least in part, by antagonizing the canonical Wnt/beta-catenin pathway [5].
• We also found that Wnt5b overexpression in 3T3-L1 preadipocytes was able to partially prevent the inhibitory effect of Wnt3a on adipogenesis [5].

References