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Orthologous residues
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EZH2 (human): S21‑p, EZH2 (mouse): S21‑p, EZH2 (rat): S21‑p
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Characterization
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Methods used to characterize site in vivo:
mutation of modification site, phospho-antibody, western blotting
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Disease tissue studied:
breast cancer
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Relevant cell lines - cell types - tissues:
293T (epithelial), 3T3 (fibroblast), A431 (epithelial), MDA-MB453 (breast cell), T47D (breast cell)
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Cellular systems studied:
cell lines
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Species studied:
human, mouse
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Enzymes shown to modify site in vitro:
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Upstream Regulation
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Potential in vivo enzymes for site:
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Type
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Enzyme
|
Evidence
|
Notes
|
|
KINASE
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Akt1 (human)
|
transfection of dominant-negative enzyme, transfection of wild-type enzyme, modification site within consensus motif, phospho-motif antibody, pharmacological inhibitor of upstream enzyme, transfection of constitutively active enzyme, co-immunoprecipitation, pharmacological activator of upstream enzyme, siRNA inhibition of enzyme
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|
|
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Treatments, proteins and their effect on site modification:
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|
Treatments
|
Referenced Treatments
|
Manipulated Protein
|
Referenced Protein
|
Effect
|
Notes
|
|
LY294002
|
|
|
|
decrease
|
|
|
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Downstream Regulation
|
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Effect of modification (function):
enzymatic activity, inhibited, molecular association, regulation
|
|
Modification regulates interactions with:
|
|
Interacting molecule
|
Interacting domains
|
Effect
|
Consequences (function)
|
Consequences (process)
|
Detection assays
|
|
H3 (human)
|
|
Disrupts
|
activation
|
transcription, altered
|
co-immunoprecipitation
|
|
|
Comments:
Phosphorylation suppresses trimethylation of Histone H3's trimethylation on K27. Enzymatic inhibition through a decreased affinity towards H3.
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