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ABL1 — CTNNB1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: CTNNB1 → ABL1 (directlyIncreases, CTNNB1 Activity)
  Evidence: The binding of beta-catenin to these partners is regulated by phosphorylation of at least three critical tyrosine residues. Each of these residues is targeted by one or more specific kinases: Y142 by Fyn, Fer and cMet; Y489 by Abl; and Y654 by Src and the epidermal growth factor receptor.
• NCI Pathway Database Posttranslational regulation of adherens junction stability and dissassembly: Slit/Robo/c-Abl/Cables complex (SLIT1-ROBO1-ABL1-CABLES1) → beta catenin (CTNNB1) (modification, activates) Rhee et al., Nat Cell Biol 2002, Rhee et al., Nat Cell Biol 2007
  Evidence: assay, physical interaction
• NCI Pathway Database Posttranslational regulation of adherens junction stability and dissassembly: Slit/Robo/c-Abl/Cables complex (SLIT1-ROBO1-ABL1-CABLES1) → N-cadherin/Ca2+/beta catenin/alpha catenin/p120 catenin complex (CDH2-CTNNB1-CTNNA1-CTNND1) (modification, activates)
  Rhee et al., Nat Cell Biol 2002, Rhee et al., Nat Cell Biol 2007
  Evidence: assay, physical interaction
• Reactome Reaction: ABL1 → CTNNB1 (reaction)
• Reactome Reaction: ABL1 → CTNNB1 (indirect_complex)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: CTNNB1 — ABL1 (physical association, affinity chromatography technology) Chen et al., Blood 2013*
• IRef Intact Interaction: CTNNB1 — ABL1 (physical association, anti bait coimmunoprecipitation) Coluccia et al., EMBO J 2007
• IRef Intact Interaction: CTNNB1 — ABL1 (phosphorylation reaction, protein kinase assay) Coluccia et al., EMBO J 2007

Text-mined interactions from Literome

Coluccia et al., EMBO J 2007 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : Bcr-Abl stabilizes beta-catenin in chronic myeloid leukemia through its tyrosine phosphorylation ... Bcr-Abl physically interacts with beta-catenin, and its oncogenic tyrosine kinase activity is required to phosphorylate beta-catenin at Y86 and Y654 residues ... These findings indicate the Bcr-Abl triggered Y phosphorylation of beta-catenin as a new mechanism responsible for its protein stabilization and nuclear signalling activation in CML
Rhee et al., Nat Cell Biol 2007 : Complex formation results in Abl mediated phosphorylation of beta-catenin on tyrosine 489, leading to a decrease in its affinity for N-cadherin, loss of N-cadherin function, and targeting of phospho-Y489-beta-catenin to the nucleus
Hu et al., PloS one 2009 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : While exerting suppressive effects on BCR-ABL , E2F1, and beta-catenin , IM/BOR and IM/PSI inhibited proteasomal degradation of protein phosphatase 2A (PP2A), leading to a re-activation of this important negative regulator of BCR-ABL