Curated Information
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PubMed Id: 18356163 
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.
McCoy CE, et al. (2008) Glucocorticoids inhibit IRF3 phosphorylation in response to Toll-like receptor-3 and -4 by targeting TBK1 activation. J Biol Chem 283, 14277-85 18356163
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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S396-p - IRF3 (human) ▲
Orthologous residues
IRF3 (human): S396‑p, IRF3 (mouse): S388‑p, IRF3 (rat): S390‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma, glioblastoma multiforme, glioma
 Relevant cell lines - cell types - tissues:  mononuclear, U373 MG (glial) [CD14 (human), transfection]
 Cellular systems studied:  cell lines, primary cells
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
LPS increase
dexamethasone LPS inhibit treatment-induced increase
poly(I-C) increase
dexamethasone poly(I-C) inhibit treatment-induced increase

T180-p - P38A (human) ▲
Orthologous residues
P38A (human): T180‑p, P38A iso2 (human): T180‑p, P38A (mouse): T180‑p, P38A (rat): T180‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma, glioblastoma multiforme, glioma
 Relevant cell lines - cell types - tissues:  mononuclear, U373 MG (glial) [CD14 (human), transfection]
 Cellular systems studied:  cell lines, primary cells
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
LPS increase
dexamethasone LPS inhibit treatment-induced increase
LPS MKP-1 (human) inhibit treatment-induced increase
poly(I-C) increase
dexamethasone poly(I-C) inhibit treatment-induced increase

Y182-p - P38A (human) ▲
Orthologous residues
P38A (human): Y182‑p, P38A iso2 (human): Y182‑p, P38A (mouse): Y182‑p, P38A (rat): Y182‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma, glioblastoma multiforme, glioma
 Relevant cell lines - cell types - tissues:  mononuclear, U373 MG (glial) [CD14 (human), transfection]
 Cellular systems studied:  cell lines, primary cells
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
LPS increase
dexamethasone LPS inhibit treatment-induced increase
LPS MKP-1 (human) inhibit treatment-induced increase
poly(I-C) increase
dexamethasone poly(I-C) inhibit treatment-induced increase

S172-p - TBK1 (human) ▲
Orthologous residues
TBK1 (human): S172‑p, TBK1 (mouse): S172‑p, TBK1 (rat): S172‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  brain cancer, glioblastoma, glioblastoma multiforme, glioma
 Relevant cell lines - cell types - tissues:  mononuclear, U373 MG (glial) [CD14 (human), transfection]
 Cellular systems studied:  cell lines, primary cells
 Species studied:  human
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
LPS increase
dexamethasone LPS inhibit treatment-induced increase
poly(I-C) increase
dexamethasone poly(I-C) inhibit treatment-induced increase


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