|
Orthologous residues
|
|
p53 (human): S20‑p, p53 (mouse): S20‑p, p53 iso2 (mouse): S23‑p, p53 (rat): S20‑p, p53 (rabbit): S20‑p, p53 (monkey): S20‑p
|
|
Characterization
|
|
Methods used to characterize site in vivo:
phospho-antibody, western blotting
|
|
Disease tissue studied:
ataxia-telangiectasia, bone cancer
|
|
Relevant cell lines - cell types - tissues:
AG1522 (fibroblast), AT1ABR (lymphoblastoid), AT5BI, U2OS (bone cell)
|
|
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
|
Chk2 (human)
|
transfection of dominant-negative enzyme
|
|
|
|
Treatments, proteins and their effect on site modification:
|
|
Treatments
|
Referenced Treatments
|
Manipulated Protein
|
Referenced Protein
|
Effect
|
Notes
|
|
ionizing radiation
|
|
|
|
increase
|
|
|
|
ionizing radiation
|
ATM (human)
|
|
inhibit treatment-induced increase
|
A-T fibroblasts
|
|
UV
|
|
|
|
increase
|
|
|
|
UV
|
ATM (human)
|
|
no effect upon treatment-induced increase
|
A-T fibroblasts
|
|
|
Downstream Regulation
|
|
Effect of modification (function):
molecular association, regulation, protein stabilization
|
|
Modification regulates interactions with:
|
|
Interacting molecule
|
Interacting domains
|
Effect
|
Consequences (function)
|
Consequences (process)
|
Detection assays
|
|
MDM2 (human)
|
|
Disrupts
|
|
|
pull-down assay
|
|
