Disease:Defects in AXIN1 are involved in hepatocellular carcinoma (HCC) [MIM:114550].,Disease:Hypermethylation of the AXIN1 promoter may be associated with caudal duplication anomaly [MIM:607864]. Caudal duplication anomaly is characterized by the occurrence of duplications of different organs in the caudal region.,Function:Controls dorsoventral patterning via two opposing effects; down-regulates beta-catenin to inhibit the Wnt signaling pathway and ventralize embryos, but also dorsalizes embryos by activating a Wnt-independent JNK signaling pathway. In Wnt signaling, probably facilitates the phosphorylation of beta-catenin and APC by GSK3B. Likely to function as a tumor suppressor. Facilitates the phosphorylation of TP53 by HIPK2 upon ultraviolet irradiation. Wild-type axin 1 can induce apoptosis in hepatocellular and colorectal cancer cells. Enhances TGF-beta signaling by recruiting the RNF111 E3 ubiquitin ligase and promoting the degradation of inhibitory SMAD7.,PTM:Probably phosphorylated by GSK3B and dephosphorylated by PP2A.,similarity:Contains 1 DIX domain.,similarity:Contains 1 RGS domain.,subunit:Homodimer (By similarity). Interacts with TP53 and HIPK2. Probably part of a complex consisting of TP53, HIPK2 and AXIN1. Interacts with glycogen synthase kinase-3 beta (GSK3B) and beta-catenin. The interaction between axin and beta-catenin occurs via the armadillo repeats contained in beta-catenin. Ternary complex. Also binds to plakoglobin (gamma-catenin), APC, DVL and PP2A. Interacts with SMAD6, SMAD7 and RNF111. Interacts with DIXDC1; prevents interaction with MAP3K1. Interacts with MAP3K4, MDFI and MDFIC. Interacts with ANKRD6. Interacts with AIDA.,tissue specificity:Ubiquitously expressed.,
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