|
Orthologous residues
|
|
COP1 (human): S387‑p, COP1 (mouse): S389‑p, COP1 (rat): S89‑p
|
|
Characterization
|
|
Methods used to characterize site in vivo:
mutation of modification site, phospho-antibody
|
|
Disease tissue studied:
ataxia-telangiectasic cancer
|
|
Relevant cell lines - cell types - tissues:
293T (epithelial), GM02052 (fibroblast), GM03490 (fibroblast), U2OS (bone cell) [GR (human)]
|
|
Cellular systems studied:
cell lines
|
|
Species studied:
human
|
|
Enzymes shown to modify site in vitro:
|
|
|
|
Upstream Regulation
|
|
Potential in vivo enzymes for site:
|
|
Type
|
Enzyme
|
Evidence
|
Notes
|
|
KINASE
|
ATM (human)
|
transfection of inactive enzyme
|
|
|
|
Treatments, proteins and their effect on site modification:
|
|
Treatments
|
Referenced Treatments
|
Manipulated Protein
|
Referenced Protein
|
Effect
|
Notes
|
|
ionizing radiation
|
|
|
|
increase
|
|
|
|
Downstream Regulation
|
|
Effect of modification (function):
intracellular localization, molecular association, regulation, protein degradation
|
|
Modification regulates interactions with:
|
|
Interacting molecule
|
Interacting domains
|
Effect
|
Consequences (function)
|
Consequences (process)
|
Detection assays
|
|
p53 (human)
|
|
Disrupts
|
protein degradation
|
|
co-immunoprecipitation
|
|
|
Comments:
phosphorylation of this site promotes COP1 autoubiquitination which prevents its interaction and stabilizes p53
|
|
Associated Diseases
|
|
Diseases:
|
Alterations:
|
Comments:
|
|
ataxia-telangiectasic cancer
|
decreased
|
alternation: mutation of ATM protein kinase
|
|
