|
Orthologous residues
|
|
GR (human): S404‑p, GR iso2 (human): S404‑p, GR (mouse): S412‑p, GR (rat): S424‑p
|
|
Characterization
|
|
Methods used to characterize site in vivo:
mass spectrometry, mutation of modification site, phospho-antibody, western blotting
|
|
Disease tissue studied:
bone cancer, liver cancer, lung cancer
|
|
Relevant cell lines - cell types - tissues:
A549 (pulmonary), HeLa (cervical), HepG2 (hepatic), MG63 (bone cell), 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
|
GSK3B (human)
|
pharmacological activator of upstream enzyme, modification site within consensus motif, transfection of constitutively active enzyme, co-immunoprecipitation, genetic knockout/knockin of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, transfection of inactive enzyme
|
|
|
|
Treatments, proteins and their effect on site modification:
|
|
Treatments
|
Referenced Treatments
|
Manipulated Protein
|
Referenced Protein
|
Effect
|
Notes
|
|
dexamethasone
|
|
|
|
increase
|
|
|
GSK-3 inhibitor X
|
dexamethasone
|
|
|
inhibit treatment-induced increase
|
|
|
|
Downstream Regulation
|
|
Effect of modification (function):
inhibition, intracellular localization, molecular association, regulation, protein conformation, protein degradation
|
|
Effect of modification (process):
apoptosis, inhibited, transcription, altered
|
|
Modification regulates interactions with:
|
|
Interacting molecule
|
Interacting domains
|
Effect
|
Consequences (function)
|
Consequences (process)
|
Detection assays
|
|
NFkB-p65 (human)
|
|
Disrupts
|
|
|
co-immunoprecipitation
|
|
p300 (human)
|
|
Induces
|
|
|
co-immunoprecipitation
|
|