Curated Information
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PubMed Id: 18326031 
Maitra S, et al. (2008) The AU-rich element mRNA decay-promoting activity of BRF1 is regulated by mitogen-activated protein kinase-activated protein kinase 2. RNA 14, 950-9 18326031
This page summarizes selected information from the record 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.
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.
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S54-p - BRF1 (human)
Orthologous residues
BRF1 (human): S54‑p, BRF1 (mouse): S54‑p, BRF1 (rat): S54‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site
 Disease tissue studied:  fibrosarcoma, fibrosarcoma of soft tissue
 Relevant cell lines - cell types - tissues:  HT1080 (fibroblast), SlowC (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE MAPKAPK2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE MAPKAPK2 (human) transfection of constitutively active enzyme, pharmacological activator of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
anisomycin increase
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  transcription, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
14-3-3 beta (human) Induces co-immunoprecipitation
 Comments:  inhibits BRF1-dependent AMD ( ARE-mediated mRNA decay)

S92-p - BRF1 (human)
Orthologous residues
BRF1 (human): S92‑p, BRF1 (mouse): S92‑p, BRF1 (rat): S92‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site
 Disease tissue studied:  fibrosarcoma, fibrosarcoma of soft tissue
 Relevant cell lines - cell types - tissues:  HT1080 (fibroblast), SlowC (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE MAPKAPK2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE MAPKAPK2 (human) transfection of constitutively active enzyme, pharmacological activator of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
anisomycin increase
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  transcription, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
14-3-3 beta (human) Induces co-immunoprecipitation
 Comments:  inhibits BRF1-dependent AMD ( ARE-mediated mRNA decay)

S203-p - BRF1 (human)
Orthologous residues
BRF1 (human): S203‑p, BRF1 (mouse): S203‑p, BRF1 (rat): S203‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site
 Disease tissue studied:  fibrosarcoma, fibrosarcoma of soft tissue
 Relevant cell lines - cell types - tissues:  HT1080 (fibroblast), SlowC (fibroblast)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE MAPKAPK2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE MAPKAPK2 (human) transfection of constitutively active enzyme, pharmacological activator of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
anisomycin increase
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  transcription, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
14-3-3 beta (human) Induces co-immunoprecipitation
 Comments:  inhibits BRF1-dependent AMD ( ARE-mediated mRNA decay)


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