is a negative regulator of the Wnt pathway, which is critical in stem cell signaling, morphogenesis, the mesenchymal-epithelial transition, and many cancers. Axin-1 functions as a tumor suppressor. Probably facilitates the phosphorylation of beta-catenin and APC by GSK3B, leading to their ubiquitination and subsequent proteolysis. Wild-type axin 1 can induce apoptosis in hepatocellular and colorectal cancer cells. Is downregulated during progression of esophageal squamous cell carcinoma. Mutation of the axin-1 gene is associated with hepatocellular carcinoma, anaplastic thyroid cancer, medulloblastoma and colorectal cancer. May have a role in oncogenesis in Hodgkin lymphoma. Axin1/2 mediate cross-talk between TGF-beta and Wnt signaling pathways. Note: This description may include information from UniProtKB.
Molecular Function: protein C-terminus binding; identical protein binding; protein homodimerization activity; protein self-association; beta-catenin binding; protein kinase binding; GTPase activator activity; protein binding; signal transducer activity; enzyme binding; ubiquitin protein ligase binding; protein complex scaffold; SMAD binding; receptor binding
Biological Process: cell death; negative regulation of Wnt receptor signaling pathway; protein polyubiquitination; apoptosis; embryonic eye morphogenesis; positive regulation of transcription, DNA-dependent; positive regulation of JNK cascade; negative regulation of protein metabolic process; nucleocytoplasmic transport; dorsal/ventral axis specification; Wnt receptor signaling pathway through beta-catenin; olfactory placode formation; activation of JNK activity; cytoplasmic microtubule organization and biogenesis; sensory perception of sound; positive regulation of ubiquitin-protein ligase activity; Wnt receptor signaling pathway involved in forebrain neuron fate commitment; protein catabolic process; protein homooligomerization; axial mesoderm formation; in utero embryonic development; positive regulation of transforming growth factor beta receptor signaling pathway; muscle cell development; negative regulation of fat cell differentiation; optic placode formation; positive regulation of peptidyl-serine phosphorylation; cellular protein complex assembly; positive regulation of protein ubiquitination; positive regulation of proteasomal ubiquitin-dependent protein catabolic process; forebrain anterior/posterior pattern formation; activation of protein kinase activity; positive regulation of protein catabolic process; positive regulation of protein amino acid phosphorylation; determination of left/right symmetry; positive regulation of GTPase activity
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.