|
Orthologous residues
|
|
CTNNB1 (human): S45‑p, CTNNB1 (mouse): S45‑p, CTNNB1 (rat): S45‑p
|
|
Characterization
|
|
Methods used to characterize site in vivo:
phospho-antibody, western blotting
|
|
Relevant cell lines - cell types - tissues:
oocyte, Rat2 (fibroblast)
|
|
Cellular systems studied:
cell lines
|
|
Species studied:
frog, rat
|
|
Enzymes shown to modify site in vitro:
|
|
|
|
Upstream Regulation
|
|
Potential in vivo enzymes for site:
|
|
Type
|
Enzyme
|
Evidence
|
Notes
|
|
KINASE
|
CK1A (rat)
|
siRNA inhibition of enzyme, transfection of wild-type enzyme
|
|
|
|
Treatments, proteins and their effect on site modification:
|
|
Treatments
|
Referenced Treatments
|
Manipulated Protein
|
Referenced Protein
|
Effect
|
Notes
|
|
lithium
|
|
|
|
increase
|
|
|
Wnt
|
|
|
|
no change compared to control
|
|
|
|
Downstream Regulation
|
|
Effect of modification (function):
molecular association, regulation, phosphorylation, protein degradation
|
|
Modification regulates interactions with:
|
|
Interacting molecule
|
Interacting domains
|
Effect
|
Consequences (function)
|
Consequences (process)
|
Detection assays
|
|
axin 1 (human)
|
|
Induces
|
|
|
electrophoretic visualization, co-immunoprecipitation
|
|
|
Comments:
CK1-A phosphorylation of S45 is required for CTNNB1 degradation and Arm degradation in drosophilla.
|
|
Associated Diseases
|
|
Diseases:
|
Alterations:
|
Comments:
|
|
colorectal cancer
|
mutation of site
|
|
|