Curated Information
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Home > Curated Information Page > PubMed Id: 17318191
Coluccia AM, et al. (2007) Bcr-Abl stabilizes beta-catenin in chronic myeloid leukemia through its tyrosine phosphorylation. EMBO J 26, 1456-66 17318191
This page summarizes selected information from the record referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.
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S33-p - CTNNB1 (human)
Modsite: QQQsyLDsGIHsGAT SwissProt Entrez-Gene
Orthologous residues
CTNNB1 (human): S33‑p, CTNNB1 (mouse): S33‑p, CTNNB1 (rat): S33‑p
Characterization
Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  leukemia, chronic myelogenous leukemia
Relevant cell lines - cell types - tissues:  BC-1 (B lymphocyte), KU812 (myeloid)
Cellular systems studied:  cell lines
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
SB216763 decrease

S37-p - CTNNB1 (human)
Modsite: yLDsGIHsGATtTAP SwissProt Entrez-Gene
Orthologous residues
CTNNB1 (human): S37‑p, CTNNB1 (mouse): S37‑p, CTNNB1 (rat): S37‑p
Characterization
Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  leukemia, chronic myelogenous leukemia
Relevant cell lines - cell types - tissues:  BC-1 (B lymphocyte), KU812 (myeloid)
Cellular systems studied:  cell lines
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
SB216763 decrease

T41-p - CTNNB1 (human)
Modsite: GIHsGATtTAPsLsG SwissProt Entrez-Gene
Orthologous residues
CTNNB1 (human): T41‑p, CTNNB1 (mouse): T41‑p, CTNNB1 (rat): T41‑p
Characterization
Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  leukemia, chronic myelogenous leukemia
Relevant cell lines - cell types - tissues:  BC-1 (B lymphocyte), KU812 (myeloid)
Cellular systems studied:  cell lines
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
SB216763 decrease

Y86-p - CTNNB1 (human)
Modsite: VADIDGQyAMTRAQR SwissProt Entrez-Gene
Orthologous residues
CTNNB1 (human): Y86‑p, CTNNB1 (mouse): Y86‑p, CTNNB1 (rat): Y86‑p
Characterization
Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  leukemia, chronic myelogenous leukemia
Relevant cell lines - cell types - tissues:  BC-1 (B lymphocyte), KU812 (myeloid)
Cellular systems studied:  cell lines
Enzymes shown to modify site in vitro
Type Enzyme
KINASE Abl (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Abl (human) co-immunoprecipitation, transfection of wild-type enzyme, mutation in upstream enzyme recognition motif
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
SB216763 increase
SB216763 Src (human) no effect upon treatment-induced increase
SKI-606 decrease
imatinib decrease
Downstream Regulation
Effect of modification (function):  molecular association, regulation, protein stabilization
Effect of modification (process):  cell growth, altered, transcription, altered
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
axin 1 (human) Disrupts co-immunoprecipitation
TCF4 (human) Induces activity, induced transcription, altered co-immunoprecipitation
Comments:  imatinib reduced tyrosine phosphorylation on CTNNB1 and promoted axin CTNNB1/GSK3B interaction.

Y142-p - CTNNB1 (human)
Modsite: AVVNLINyQDDAELA SwissProt Entrez-Gene
Orthologous residues
CTNNB1 (human): Y142‑p, CTNNB1 (mouse): Y142‑p, CTNNB1 (rat): Y142‑p
Characterization
Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  leukemia, chronic myelogenous leukemia
Relevant cell lines - cell types - tissues:  BC-1 (B lymphocyte), KU812 (myeloid)
Cellular systems studied:  cell lines
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
SB216763 increase
SB216763 Src (human) no effect upon treatment-induced increase
SKI-606 decrease
imatinib decrease

Y654-p - CTNNB1 (human)
Modsite: RNEGVAtyAAAVLFR SwissProt Entrez-Gene
Orthologous residues
CTNNB1 (human): Y654‑p, CTNNB1 (mouse): Y654‑p, CTNNB1 (rat): Y654‑p
Characterization
Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  leukemia, chronic myelogenous leukemia
Relevant cell lines - cell types - tissues:  BC-1 (B lymphocyte), KU812 (myeloid)
Cellular systems studied:  cell lines
Enzymes shown to modify site in vitro
Type Enzyme
KINASE Abl (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Abl (human) co-immunoprecipitation, transfection of wild-type enzyme, mutation in upstream enzyme recognition motif
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
SB216763 increase
SB216763 Src (human) no effect upon treatment-induced increase
SKI-606 decrease
imatinib decrease
Downstream Regulation
Effect of modification (function):  molecular association, regulation, protein stabilization
Effect of modification (process):  cell growth, altered, transcription, altered
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
axin 1 (human) Disrupts co-immunoprecipitation
TCF4 (human) Induces activity, induced transcription, altered co-immunoprecipitation
Comments:  imatinib reduced tyrosine phosphorylation on CTNNB1 and promoted axin CTNNB1/GSK3B interaction.

Y216-p - GSK3B (human)
Modsite: RGEPNVsyICsRyyR SwissProt Entrez-Gene
Orthologous residues
GSK3B (human): Y216‑p, GSK3B iso2 (human): Y216‑p, GSK3B (mouse): Y216‑p, GSK3B (rat): Y216‑p, GSK3B (rabbit): Y216‑p
Downstream Regulation
Effect of modification (function):  molecular association, regulation, protein stabilization
Effect of modification (process):  cell growth, altered, transcription, altered
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
TCF4 (human) Induces activity, induced transcription, altered co-immunoprecipitation
axin 1 (human) Disrupts co-immunoprecipitation
Comments:  imatinib reduced tyrosine phosphorylation on CTNNB1 and promoted axin CTNNB1/GSK3B interaction.

Y419-p - Src (human)
Modsite: RLIEDNEytARQGAk SwissProt Entrez-Gene
Orthologous residues
Src (human): Y419‑p, Src iso2 (human): Y425‑p, Src (mouse): Y424‑p, Src iso2 (mouse): Y418‑p, Src (rat): Y419‑p, Src (chicken): Y416‑p
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
SKI-606 decrease
imatinib decrease
SU6656 decrease