Extended Data Fig. 6: β-catenin forms repressive complexes with Ikaros and NuRD factors in B-cells.
(a-c) Human B-ALL (MXP2), B-cell lymphoma (JEKO), AML (MOLM13), colon cancer (SW480) and lung cancer (H446) cell lines were engineered with β-catenin mutations impairing GSK3B and CK1a-mediated phosphorylation. (a) Proteins bound to β-catenin were identified by mass-spectrometry following Co-IP with antibodies against β-catenin or control Ig. β-catenin binding proteins in each cell type were plotted as a function of background binding (x-axis, non-specific binding defined by CRAPOME database) and log2-fold enrichment over control Ig (y-axis). (b) Western blot was performed to validate β-catenin-binding of Ikaros factors IKZF1, IKZF2, IKZF3 and NuRD complex component MTA2, as well as AXIN1 (positive control) using input lysates and elutes from the Co-IP experiments with antibodies against β-catenin or control Ig (n = 2 biological replicates). (c) Principal component analysis corroborated B-lymphoid-specific (B-ALL, B-cell lymphoma) β-catenin-interactomes that were clustered together along PC1 axis and separated from myeloid, colon and lung epithelial cells.
