|
Orthologous residues
|
|
p53 (human): S15‑p, p53 (mouse): S15‑p, p53 iso2 (mouse): S18‑p, p53 (rat): S15‑p, p53 (rabbit): S15‑p, p53 (monkey): S15‑p
|
|
Characterization
|
|
Methods used to characterize site in vivo:
immunoprecipitation, phospho-antibody
|
|
Relevant cell lines - cell types - tissues:
AT1ABR (lymphoblastoid), C3ABR (lymphoblastoid)
|
|
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)
|
genetic knockout/knockin of upstream enzyme, activation of upstream enzyme
|
in patients diagnosed with Ataxia-Telangiectasia
|
|
|
Treatments, proteins and their effect on site modification:
|
|
Treatments
|
Referenced Treatments
|
Manipulated Protein
|
Referenced Protein
|
Effect
|
Notes
|
|
Cd(2+)
|
|
|
|
increase
|
|
|
ionizing radiation
|
|
|
|
increase
|
|
|
Cd(2+), ionizing radiation
|
|
|
|
augment treatment-induced increase
|
|
|
Cd(2+), siRNA, ionizing radiation
|
|
|
|
inhibit treatment-induced increase
|
|
|
Cd(2+), ALLN, ionizing radiation
|
|
|
|
augment treatment-induced increase
|
|
|
Cd(2+), ALLN, siRNA, ionizing radiation
|
|
|
|
inhibit treatment-induced increase
|
|
|
