Curated Information
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Curated Information Page
PubMed Id: 15383283 
This page summarizes selected information from the article referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
Wu RC, et al. (2004) Selective phosphorylations of the SRC-3/AIB1 coactivator integrate genomic reponses to multiple cellular signaling pathways. Mol Cell 15, 937-49 15383283
Only sites from this record are displayed on this page. Click on the protein name to open the protein page, and on the RSD number to open the site page. For the complete dataset, click the download button, on the right.
Download Sites

T24-p - SRC-3 (human) ▲
Orthologous residues
SRC‑3 (human): T24‑p, SRC‑3 (mouse): A25‑p, SRC‑3 (rat): ‑
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial), HeLa (cervical), MEF (fibroblast) [SRC-3 (human)]
 Cellular systems studied:  cell lines
 Species studied:  mouse
 Comments:  NCoA3 -/- +/+ MEFs were used to define physiological functions of NCoA3. NCoA3 is required for IL-6 mRNA induction. Reconstitution of wild-type NCoA3 restored IL-6 production by TNF. NCoA3 -/- MEFs were used to determine oncogenic potential of NCoA3using colony focus formation assays, expressing mutated sites and Ras V12.
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE JNK1 (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
estrogen ER-alpha (human) increase
siRNA decrease siRNA knockdown of kinases reduced phosphorylation of sites.
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
ER-alpha (human) Disrupts activation co-immunoprecipitation
 Comments:  Mutations to alanine inhibited protein-protein interactions.

S505-p - SRC-3 (human) ▲
Orthologous residues
SRC‑3 (human): S505‑p, SRC‑3 (mouse): S498‑p, SRC‑3 (rat): S205‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial), HeLa (cervical), MEF (fibroblast) [SRC-3 (human)]
 Cellular systems studied:  cell lines
 Species studied:  mouse
 Comments:  NCoA3 -/- +/+ MEFs were used to define physiological functions of NCoA3. NCoA3 is required for IL-6 mRNA induction. Reconstitution of wild-type NCoA3 restored IL-6 production by TNF. NCoA3 -/- MEFs were used to determine oncogenic potential of NCoA3using colony focus formation assays, expressing mutated sites and Ras V12.
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE JNK1 (human)
KINASE p38-alpha (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
estrogen ER-alpha (human) increase
siRNA decrease siRNA knockdown of kinases reduced phosphorylation of sites.
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
ER-alpha (human) Disrupts activation co-immunoprecipitation
 Comments:  Mutations to alanine inhibited protein-protein interactions.

S543-p - SRC-3 (human) ▲
Orthologous residues
SRC‑3 (human): S543‑p, SRC‑3 (mouse): S536‑p, SRC‑3 (rat): S243‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial), HeLa (cervical), MEF (fibroblast) [SRC-3 (human)]
 Cellular systems studied:  cell lines
 Species studied:  mouse
 Comments:  NCoA3 -/- +/+ MEFs were used to define physiological functions of NCoA3. NCoA3 is required for IL-6 mRNA induction. Reconstitution of wild-type NCoA3 restored IL-6 production by TNF. NCoA3 -/- MEFs were used to determine oncogenic potential of NCoA3using colony focus formation assays, expressing mutated sites and Ras V12.
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE JNK1 (human)
KINASE p38-alpha (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
estrogen ER-alpha (human) increase
siRNA decrease siRNA knockdown of kinases reduced phosphorylation of sites.
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
ER-alpha (human) Disrupts activation co-immunoprecipitation
 Comments:  Mutations to alanine inhibited protein-protein interactions.

S857-p - SRC-3 (human) ▲
Orthologous residues
SRC‑3 (human): S857‑p, SRC‑3 (mouse): S847‑p, SRC‑3 (rat): S551‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial), HeLa (cervical), MEF (fibroblast) [SRC-3 (human)]
 Cellular systems studied:  cell lines
 Species studied:  mouse
 Comments:  NCoA3 -/- +/+ MEFs were used to define physiological functions of NCoA3. NCoA3 is required for IL-6 mRNA induction. Reconstitution of wild-type NCoA3 restored IL-6 production by TNF. NCoA3 -/- MEFs were used to determine oncogenic potential of NCoA3using colony focus formation assays, expressing mutated sites and Ras V12.
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE IKK-alpha (human)
KINASE PKACa (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
estrogen ER-alpha (human) increase
siRNA decrease siRNA knockdown of kinases reduced phosphorylation of sites.
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
ER-alpha (human) Disrupts activation co-immunoprecipitation
 Comments:  Mutations to alanine inhibited protein-protein interactions.

S860-p - SRC-3 (human) ▲
Orthologous residues
SRC‑3 (human): S860‑p, SRC‑3 (mouse): S850‑p, SRC‑3 (rat): S554‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial), HeLa (cervical), MEF (fibroblast) [SRC-3 (human)]
 Cellular systems studied:  cell lines
 Species studied:  mouse
 Comments:  NCoA3 -/- +/+ MEFs were used to define physiological functions of NCoA3. NCoA3 is required for IL-6 mRNA induction. Reconstitution of wild-type NCoA3 restored IL-6 production by TNF. NCoA3 -/- MEFs were used to determine oncogenic potential of NCoA3using colony focus formation assays, expressing mutated sites and Ras V12.
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE p38-alpha (human)
KINASE JNK1 (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
estrogen ER-alpha (human) increase
siRNA decrease siRNA knockdown of kinases reduced phosphorylation of sites.
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
ER-alpha (human) Disrupts activation co-immunoprecipitation
 Comments:  Mutations to alanine inhibited protein-protein interactions.

S867-p - SRC-3 (human) ▲
Orthologous residues
SRC‑3 (human): S867‑p, SRC‑3 (mouse): G857‑p, SRC‑3 (rat): V561‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  293 (epithelial), HeLa (cervical), MEF (fibroblast) [SRC-3 (human)]
 Cellular systems studied:  cell lines
 Species studied:  mouse
 Comments:  NCoA3 -/- +/+ MEFs were used to define physiological functions of NCoA3. NCoA3 is required for IL-6 mRNA induction. Reconstitution of wild-type NCoA3 restored IL-6 production by TNF. NCoA3 -/- MEFs were used to determine oncogenic potential of NCoA3using colony focus formation assays, expressing mutated sites and Ras V12.
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE p38-alpha (human)
KINASE JNK1 (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
estrogen ER-alpha (human) increase
siRNA decrease siRNA knockdown of kinases reduced phosphorylation of sites.
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
ER-alpha (human) Disrupts activation co-immunoprecipitation
 Comments:  Mutations to alanine inhibited protein-protein interactions.


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