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Home > Curated Information Page > PubMed Id: 25500543
Lemieux E, et al. (2015) Oncogenic KRAS signalling promotes the Wnt/β-catenin pathway through LRP6 in colorectal cancer. Oncogene 34, 4914-27 25500543
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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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 phospho-antibody, western blotting
Disease tissue studied:  colorectal cancer, colorectal carcinoma
Relevant cell lines - cell types - tissues:  colon, DLD1 (intestinal), HT-29 (intestinal), IEC-6 (epithelial)
Cellular systems studied:  cell lines, tissue
Species studied:  human, mouse, rat
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
U0126 no change compared to control

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 phospho-antibody, western blotting
Disease tissue studied:  colorectal cancer, colorectal carcinoma
Relevant cell lines - cell types - tissues:  colon, DLD1 (intestinal), HT-29 (intestinal), IEC-6 (epithelial)
Cellular systems studied:  cell lines, tissue
Species studied:  human, mouse, rat
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
U0126 no change compared to control

S552-p - CTNNB1 (human)
Modsite: QDtQRRtsMGGtQQQ SwissProt Entrez-Gene
Orthologous residues
CTNNB1 (human): S552‑p, CTNNB1 (mouse): S552‑p, CTNNB1 (rat): S552‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  colorectal cancer, colorectal carcinoma
Relevant cell lines - cell types - tissues:  colon, DLD1 (intestinal), HT-29 (intestinal), IEC-6 (epithelial)
Cellular systems studied:  cell lines, tissue
Species studied:  human, mouse, rat
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
U0126 no change compared to control

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 phospho-antibody, western blotting
Disease tissue studied:  colorectal cancer, colorectal carcinoma
Relevant cell lines - cell types - tissues:  colon, DLD1 (intestinal), HT-29 (intestinal), IEC-6 (epithelial)
Cellular systems studied:  cell lines, tissue
Species studied:  human, mouse, rat
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
U0126 no change compared to control

S1490-p - LRP6 (human)
Modsite: AILNPPPsPAtERsH SwissProt Entrez-Gene
Orthologous residues
LRP6 (human): S1490‑p, LRP6 (mouse): S1490‑p, LRP6 (rat):
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  colorectal cancer, colorectal carcinoma
Relevant cell lines - cell types - tissues:  colon, DLD1 (intestinal), HT-29 (intestinal), IEC-6 (epithelial)
Cellular systems studied:  cell lines, tissue
Species studied:  human, mouse, rat
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ERK1 (human) phospho-antibody, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
BRAF (human) increase
U0126 4-HT BRAF (human) inhibit treatment-induced increase
PD184352 4-HT BRAF (human) inhibit treatment-induced increase
SCH772984 decrease
SP600125 decrease
SB216763 no change compared to control
KRas (human) increase
4-HT increase
Downstream Regulation
Effect of modification (function):  activity, induced
Effect of modification (process):  signaling pathway regulation, transcription, induced
Comments:  increased B-catennin/TCF4 activity
Associated Diseases
Diseases Alterations Comments
colorectal carcinoma increased

T1572-p - LRP6 (human)
Modsite: EPVPPPPtPRsQyLs SwissProt Entrez-Gene
Orthologous residues
LRP6 (human): T1572‑p, LRP6 (mouse): T1572‑p, LRP6 (rat):
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  colorectal cancer, colorectal carcinoma
Relevant cell lines - cell types - tissues:  colon, DLD1 (intestinal), HT-29 (intestinal), IEC-6 (epithelial)
Cellular systems studied:  cell lines, tissue
Species studied:  human, mouse, rat
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ERK1 (human) phospho-antibody, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
BRAF (human) increase
U0126 4-HT BRAF (human) inhibit treatment-induced increase
PD184352 4-HT BRAF (human) inhibit treatment-induced increase
SCH772984 decrease
SP600125 decrease
SB216763 no change compared to control
KRas (human) increase
4-HT increase
Downstream Regulation
Effect of modification (function):  activity, induced
Effect of modification (process):  signaling pathway regulation, transcription, induced
Comments:  increased B-catennin/TCF4 activity
Associated Diseases
Diseases Alterations Comments
colorectal carcinoma increased