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ABL1 — CTNND1
Pathways - manually collected, often from reviews:
-
NCI Pathway Database Posttranslational regulation of adherens junction stability and dissassembly:
Slit/Robo/c-Abl/Cables complex (SLIT1-ROBO1-ABL1-CABLES1)
→
N-cadherin/p120 catenin complex (CDH2-CTNND1)
(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
Text-mined interactions from Literome
Kain et al., Oncogene 2003
(Carcinoma...) :
c-Abl induced disruption of
Crk/CAS complexes inhibits cell migration and promotes apoptosis in normal cells, and is deregulated in highly invasive carcinoma cells
Anfinogenova et al., Circ Res 2007
:
These results suggest that
Abl may
play a pivotal role in mediating
CAS phosphorylation, the assembly of the multiprotein complex, actin assembly, and constriction in resistance arteries
Jia et al., Am J Physiol Cell Physiol 2010
:
Abl activation
regulates the dissociation of CAS from cytoskeletal vimentin by modulating
CAS phosphorylation in smooth muscle ... Inhibition of
Abl phosphorylation by the decoy peptide
attenuated the agonist induced phosphorylation of
Crk associated substrate (CAS) , an adapter protein participating in the signaling processes that regulate force development in smooth muscle ... These results suggest that
Abl regulates the dissociation of CAS from the vimentin network, actin polymerization, and contraction by modulating
CAS phosphorylation in smooth muscle