Curated Information
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PubMed Id: 10195894 
Delhase M, Hayakawa M, Chen Y, Karin M (1999) Positive and negative regulation of IkappaB kinase activity through IKKbeta subunit phosphorylation. Science 284, 309-13 10195894
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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S176-p - IKKA (human)
Orthologous residues
IKKA (human): S176‑p, IKKA (mouse): S176‑p, IKKA (rat): S176‑p
Characterization
 Methods used to characterize site in vivo [32P] bio-synthetic labeling, immunoprecipitation, mutation of modification site, phosphoamino acid analysis, phosphopeptide mapping
 Relevant cell lines - cell types - tissues:  293 (epithelial), HeLa (cervical), HT-29 (intestinal)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Nik (human) transfection of constitutively active enzyme, transfection of inactive enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IL-1b increase
TNF increase

S180-p - IKKA (human)
Orthologous residues
IKKA (human): S180‑p, IKKA (mouse): S180‑p, IKKA (rat): S180‑p
Characterization
 Methods used to characterize site in vivo [32P] bio-synthetic labeling, immunoprecipitation, mutation of modification site, phosphoamino acid analysis, phosphopeptide mapping
 Relevant cell lines - cell types - tissues:  293 (epithelial), HeLa (cervical), HT-29 (intestinal)
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Nik (human) transfection of constitutively active enzyme, transfection of inactive enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IL-1b increase
TNF increase

S177-p - IKKB (human)
Orthologous residues
IKKB (human): S177‑p, IKKB (mouse): S177‑p, IKKB (rat): S177‑p
Characterization
 Methods used to characterize site in vivo [32P] bio-synthetic labeling, mutation of modification site, phosphopeptide mapping
 Relevant cell lines - cell types - tissues:  HeLa (cervical) [IKKB (human)], HeLa (cervical) [Nik (human)], HT-29 (intestinal) [IKKB (human)], HT-29 (intestinal) [Nik (human)]
 Cellular systems studied:  cell lines
 Species studied:  human
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Nik (human)
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
TNF increase
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced
 Comments:  A S177A mutation slightly decreased enzymatic activity; replacement of both S181 and S177 abolished IKK activation.

S181-p - IKKB (human)
Orthologous residues
IKKB (human): S181‑p, IKKB (mouse): S181‑p, IKKB (rat): S181‑p
Characterization
 Methods used to characterize site in vivo [32P] bio-synthetic labeling, mutation of modification site, phosphopeptide mapping
 Relevant cell lines - cell types - tissues:  HT-29 (intestinal) [IKKB (human)], HT-29 (intestinal) [Nik (human)]
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Nik (human)
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
TNF increase
IL-1b increase
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced
 Comments:  A S181A mutation severely inhibited enzymatic activity; replacement of both S181 and S177 abolished IKK activation.


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