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CTNNB1 — WNT5A

Text-mined interactions from Literome

Schulte et al., J Neurochem 2005 : Using a substantia nigra derived dopaminergic cell line ( SN4741 ), we found that Wnt-5a , unlike Wnt-3a, did not promote beta-catenin phosphorylation or stabilization
Behbod et al., Stem Cells 2006 : Accordingly, a smaller percentage of MG-SPs expressed nuclear beta-catenin , possibly as a consequence of the higher expression of Wnt-5a
Mikels et al., PLoS Biol 2006 : We show that in addition to its inhibitory function, Wnt5a can also activate beta-catenin signaling in the presence of the appropriate Frizzled receptor, Frizzled 4
Ryu et al., J Biol Chem 2006 : Wnt-5a and Wnt-11 did not cause accumulation of beta-catenin or activation of the beta-catenin-Tcf/Lef transcriptional complex
Bryja et al., J Cell Sci 2007 : As expected, Wnt-5a blocked the Wnt-3a induced activation of beta-catenin
Torii et al., Cell Signal 2008 : In addition, Wnt5a increased the nuclear beta-catenin level and treatment with imatinib or ionomycin, either of which blocks the beta-catenin pathway, reduced the anti-apoptotic activity of Wnt5a, together suggesting the simultaneous involvement of the beta-catenin mediated pathway in the Wnt5a anti-apoptotic activity
Roarty et al., Breast Cancer Res 2009 (Mammary Neoplasms, Experimental) : Loss of TGF-beta or Wnt5a signalling resulted in stabilisation of nuclear beta-catenin and expression of Wnt/beta-catenin target genes suggesting that TGF-beta and Wnt5a act to inhibit Wnt/beta-catenin signalling in mammary epithelium ... The key findings here are that : TGF-beta and Wnt5a regulate Wnt/beta-catenin activity ; and loss of TGF-beta and Wnt5a redirect the phenotype of tumours so that they resemble tumours induced by activation of Wnt/beta-catenin
Incassati et al., Breast Cancer Res 2009 (Breast Neoplasms...) : Here, they show that inhibition of stromal TGF-beta signaling or Wnt5a loss leads to increased beta-catenin transcriptional activity and reduced latency in mammary tumor models, with tumors displaying a higher proportion of progenitor cell markers
Ge et al., Arthritis Rheum 2009 : Wnt-5A did not cause accumulation and nuclear translocation of beta-catenin or activation of the beta-catenin-Tcf/Lef transcription complex
Mikels et al., J Biol Chem 2009 : Emerging evidence suggests that Wnt5a can inhibit Wnt/beta-catenin signaling through interaction with the receptor Ror2
Verkaar et al., FASEB J 2010 : Using the assay, we confirmed that Wnt-5a represses beta-catenin-driven reporter gene activity downstream of nuclear entry of beta-catenin