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SOX9 — WNT11

Text-mined interactions from Literome

Dong et al., J Cell Physiol 2006 (Hypertrophy) : Wnt8c and Wnt9a strongly inhibited mRNA levels of Sox9 and type II collagen ( col2a1 ) ... Wnt8c further enhanced canonical bone morphogenetic proteins ( BMP-2 ) -induced expression of Runx2 and col10a1 while Wnt8c and Wnt9a inhibited TGF-beta induced expression of Sox9 and col2a1
Wang et al., Cancer Res 2007 (Neoplasm Recurrence, Local...) : SOX9 message and protein levels in prostate cancer cells were increased by treatment with glycogen synthase kinase 3beta inhibitor ( SB415286 ), and SOX9 was reduced when beta-catenin was down-regulated by small interfering RNA ( siRNA ), indicating that SOX9 expression in prostate cancer is regulated by Wnt/beta-catenin signaling
Topol et al., J Biol Chem 2009 : Sox9 inhibits Wnt signaling by promoting beta-catenin phosphorylation in the nucleus ... Chondrocyte fate determination and maintenance requires Sox9 , an intrinsic transcription factor, but is inhibited by Wnt/beta-catenin signaling activated by extrinsic Wnt ligands
Kormish et al., Dev Dyn 2010 (Neoplasms) : In some contexts, Wnt signaling also regulates SOX expression resulting in feedback regulatory loops that fine-tune cellular responses to beta-catenin/TCF activity
Bernard et al., Endocrinology 2012 : Wnt signaling in ovarian development inhibits Sf1 activation of Sox9 via the Tesco enhancer ... Ectopic activation of Wnt/ß-catenin signaling in male gonads led to a loss of Sf1 binding to the Tesco enhancer and absent Sox9 expression that we also observed in wild-type ovaries ... Moreover, ectopic Wnt/ß-catenin signaling induced the expression of the female somatic cell markers, Bmp2 and Rspo1, as a likely consequence of Sox9 loss
Wang et al., J Biol Chem 2013 (Breast Neoplasms...) : Consistently, SOX9 overexpression in BCa cell lines and transgenic SOX9 expression in breast epithelium caused increased LRP6 and TCF4 expression and Wnt/ß-catenin activation ... These results identify SOX9 mediated Wnt/ß-catenin activation as one of the molecular mechanisms underlying aberrant Wnt/ß-catenin activity in BCa, especially in the BL-BCa subgroup